ACUTE CARE INTERVENTIONS OF BRAIN

NEUROSCIENCE CRITICAL CARE

JASSIN M. JOURIA, MD

Dr. Jassin M. Jouria is a practicing Emergency , professor of academic medicine, and medical author. He graduated from Ross University School of Medicine and has completed his clinical clerkship training in various teaching hospitals throughout New York, including King’s County Hospital Center and Brookdale Medical Center, among others. Dr. Jouria has passed all USMLE medical board exams, and has served as a test prep tutor and instructor for Kaplan. He has developed several medical courses and curricula for a variety of educational institutions. Dr. Jouria has also served on multiple levels in the academic field including faculty member and Department Chair. Dr. Jouria continues to serve as a Subject Matter Expert for several continuing education organizations covering multiple basic medical sciences. He has also developed several continuing courses covering various topics in clinical medicine. Recently, Dr. Jouria has been contracted by the University of Miami/Jackson Memorial Hospital’s Department of to develop an e-module training series for trauma patient management. Dr. Jouria is currently authoring an academic textbook on Human Anatomy & Physiology.

ABSTRACT

Brain injuries can be devastating and their impact is frequently felt deeply by family and friends as well as the patient. The trauma of a brain can continue not just in the initial days and weeks after occurrence but for months and years afterward. The neuroscience critical care team caring for a patient immediately following a traumatic event involving brain injury can have a profound impact on the patient’s outcome and quality of life.

1 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Policy Statement

This activity has been planned and implemented in accordance with the policies of NurseCe4Less.com and the continuing nursing education requirements of the American Nurses Credentialing Center's Commission on Accreditation for registered nurses. It is the policy of NurseCe4Less.com to ensure objectivity, transparency, and best practice in clinical education for all continuing nursing education (CNE) activities.

Continuing Education Credit Designation

This educational activity is credited for 3 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity.

Statement of Learning Need

Clinicians need to understand the different types of treatment a patient with an acute brain injury may receive. Because the treatment for will differ depending on the severity and type of injury, patient care will need to be individualized. Treatment goals for each type of head injury need to be identified by the full neuroscience treatment team.

Course Purpose

To provide health clinicians with knowledge of the types and treatment of acute brain injury.

2 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Target Audience

Advanced Practice Registered Nurses and Registered Nurses

(Interdisciplinary Health Team Members, including Vocational Nurses and Medical Assistants may obtain a Certificate of Completion)

Course Author & Planning Team Conflict of Interest Disclosures

Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA

Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures

Acknowledgement of Commercial Support

There is no commercial support for this course.

Please take time to complete a self-assessment of knowledge, on page 4, sample questions before reading the article. Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course.

3 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 1. When swelling and fluid accumulation occur within the brain, it can be extremely dangerous for the patient primarily because this accumulation

a. creates lesions within the brain. b. creates pressure in the brain. c. blocks the brain-blood barrier. d. may lead to .

2. True or False: Once (ICP) becomes elevated, the only option for treatment is a ventriculostomy.

a. True b. False

3. Patients with low risk head injuries may display symptoms such as

a. persistent emesis. b. severe headache. c. anterograde amnesia. d. None of the above

4. When a patient is released to a caregiver for monitoring the injury at home, the home caregiver should

a. check the patient once a day. b. assess the patient every two hours. c. assess the patient each morning. d. take the patient for outpatient assessment.

5. Cranial nerve and pupillary examination includes assessing a patient’s

a. level of consciousness. b. posture. c. gag reflex. d. pain sensations.

4 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Introduction

The intensive care management of patients with a brain injury is a dynamic process, and starts in the pre-hospital period. During the early stages of hospital care, the patients may be managed in a variety of locations including the emergency department, department, and the operating room before they are admitted to the intensive care unit (ICU). The continuum of acute care, during the golden hour, from the time of injury through the start of definitive care, should be ensured and based on established medical guidelines and recommendations. The fundamental principles of critical care management of patients with a brain injury in the acute phases of hospital care are raised in the following sections.

Critical Care Strategies In The Neuroscience Unit

An initial assessment and diagnostic imaging are used to determine the level of severity of a brain injury and to determine any specific complications. Once this information is obtained, and the patient is stabilized, medical personnel can begin to treat specific injuries. Treatment is individualized based on the injuries and the severity of the damage.

In some instances, a patient with head trauma may require initial surgical interventions. These surgical interventions are conducted immediately following the initial assessment and treatment to minimize some of the immediate complications that are most dangerous or threatening to the patient.35 When a patient requires an initial surgical intervention, he or she is typically admitted to the intensive care unit for further treatment and monitoring. Initial surgical interventions are used to remove or repair hematomas and contusions.66

5 nursece4less.com nursece4less.com nursece4less.com nursece4less.com A patient may experience swelling in the brain. When this occurs, fluid accumulates within the brain and pressure begins to build. This causes additional swelling and disruption to the fluid balance.45 With injuries to other parts of the body, swelling and fluid accumulation is normal and may pose little risk; however, when swelling and fluid accumulation occur within the brain, it can be extremely dangerous for the patient. The danger arises because the limits the space for the brain to expand so that swelling and fluid accumulation elevates intracranial pressure (ICP).11

When a patient is evaluated with swelling in the brain, it is necessary to monitor the swelling to ensure that it does not cause additional damage. This is accomplished using a probe or catheter.66 The instrument is inserted into the skull and is placed at the subarachnoid level to ensure accurate measurements. Once the instrument is properly placed, it is connected to a monitor that displays information regarding the patient’s ICP. This information is closely monitored so that action can be taken if the ICP reaches an alarming level.28 If this occurs, the patient may have to undergo a ventriculostomy. This procedure is used to drain cerebrospinal fluid as a way to reduce pressure on the brain.30 In some instances, pharmacological agents may be used to decrease ICP. These drugs include mannitol and barbiturates.66

While the above information provides an overview of the different types of treatment a patient may receive, it is important to note that the treatment for head injury will differ depending on the severity and type of injury. A patient will require different care for a penetrating head injury than a blunt head injury. In addition, a mild head injury will be treated differently than a severe head injury. It is important to understand the treatment goals for each type of injury.

6 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Mild, Moderate or Severe Head Injuries

When a patient experiences a mild head injury, minimal treatment is required. Most mild head injuries will resolve on their own and will not progress in severity.114 However, there is a chance that the head injury can progress to a more serious injury.71 During the initial assessment, the risk level of the head injury will be assessed and it will be categorized as either low risk or moderate risk.18 Low Risk injuries typically include symptoms of headaches, dizziness, and nausea.115

Patients who display symptoms of low risk injuries will not require extensive treatment. They rarely require the level of assessment that moderate or high risk patients do, and it is not common to utilize radiologic imaging to evaluate the injury.116 In most instances, patients will be released and will require monitoring at home until the window for developing additional injuries has passed.117 When a patient is released, thorough instructions should be given to the patient and caregivers for monitoring the injury at home. The home caregiver should wake the patient every two hours to provide a thorough assessment. Caregivers should watch for symptoms in the patient of severe headaches, persistent nausea, vomiting, seizures, confusion, unusual behavior, and watery discharge from the nose or .110

Moderate risk injuries typically include the following symptoms of persistent emesis, severe headache, anterograde amnesia, loss of consciousness, and signs of intoxication.118 When a patient shows signs of a moderate risk head injury, assessment should be made using a computed tomography (CT) scan. Once the CT scan findings are reviewed, the patient is eligible for release, assuming the findings were clear. However, patients must be observed for at least eight hours prior to being released.104 Patients who have moderate to severe brain injuries will require treatment beyond an

7 nursece4less.com nursece4less.com nursece4less.com nursece4less.com initial observation and release. Treatment will depend on the type, location and severity of the injury. However, in most instances, treatment will follow an initial standard set of procedures before being tailored to the specific needs of the patient. General guidelines for initial patient treatment are discussed below.

Assessment

Assessment and treatment of (TBI) should begin as soon as possible. Therefore, emergency personnel are often the first individuals who assess and treat the injury.66 Typically, treatment begins as soon as emergency responders arrive on the scene or as soon as an individual arrives at the emergency room. Initial that is caused by trauma cannot be reversed. So, initial treatment involves stabilizing the patient and administering treatment that will prevent further damage.28 The key components of the trauma assessment include the airway assessment, skull examination, patient history, and neurological examination.26

Assessment of Airway:

Assessment of the patient’s airway involves stabilization of the cervical spine, breathing, circulation, heart rate and blood pressure before the neurological exam.

Examination of the Skull:

Examination of the skull involves assessment for periorbital and postauricular ecchymosis, cerebrospinal fluid otorrhea and rhinorrhea, hemotympanum, penetrating injury or depressed fracture, and lacerations.

8 nursece4less.com nursece4less.com nursece4less.com nursece4less.com History:

Gathering information related to the mechanism of injury and care prior to hospitalization are outlined below.

Neurological Exam Cerebral Function Assess the level of consciousness, mental status, awareness, arousal, cognitive function, and behavior.

Cranial Nerve and This reflects brainstem function. Assess the pupils, eye Pupillary movements, cough reflex, corneal reflex and gag reflex. Examination

Motor and Assess strength, movement, gait, and posture. Each extremity Cerebellar must be assessed separately. It is important to document the Function degree and type of stimulus applied to elicit the motor activity. Central stimuli include sternal rub, trapezius pinch and/or supraorbital pressure. Abnormal findings include abnormal posturing, flaccidity, and focal motor movements.

Sensory Assess tactile and pain sensations. Examination Reflex Assess superficial and deep tendon reflexes. Examination Glasgow Coma This is a valuable component of the neurological exam because Scale it is nationally and internationally recognized. It is only one part of the neurological exam.

Severe Head Injury: GCS # 8 or a decrease in 2 points or more after admission. Moderate Head Injury: GCS 9-12 Mild Head Injury: GCS 13-15

Due to the diverse causes of head injury and the differing needs of patients, initial contact with the patient involves an assessment of the cause of the injury and a screening to determine the extent of the injuries.28 This is important, as the mechanism of injury will determine the type of treatment needed. For example, blast trauma related head trauma is more complex than other forms of head trauma.119 Due to the complexity of blast related

9 nursece4less.com nursece4less.com nursece4less.com nursece4less.com head injury, the assessment and treatment can be difficult to administer and determine. Therefore, in combat, it is more common to evaluate all service members who have been exposed to a blast and identify those that present symptoms of head injury.119 However, in civilian instances of head trauma, it is more common to assess each patient individually based on the symptoms present as non-blast related causes of head trauma tend to be less complicated.28

Prior to conducting a full assessment of an individual who is suspected of having a traumatic brain injury, the primary concern is ensuring that the patient is stabilized and that any further injury is prevented. During the initial stage of contact, medical personnel are primarily concerned with ensuring that the patient has a proper supply of oxygen to the brain and the rest of the body.120 Another priority is to maintain an adequate blood flow while controlling blood pressure. This will help stabilize the patient while minimizing further damage to the brain.28

The Glasgow Coma Scale

Once a patient is stabilized, medical personnel will assess the patient and determine the extent of the injury. Primary assessment includes measuring vital signs and reflexes, as well as administering a thorough neurological exam. The initial exam includes checking the patient’s temperature, blood pressure, pulse, breathing rate, pupil size and response to light.23

After the vital signs and basic neurologic functions are assessed, the emergency medical clinician will assess the patient’s level of consciousness and neurologic functioning. This assessment is done using the Glasgow Coma Scale, which is a standardized, 15-point test that measures neurologic functioning using three assessments: eye opening, best verbal response,

10 nursece4less.com nursece4less.com nursece4less.com nursece4less.com and best motor response. These measures are used to determine the severity of the brain injury. A score of 13 to 15 is classified as mild, 9 to 12 as moderate, and 3 to 8 as severe. Though well-known and widely used, this classification scheme is most useful in predicting acute survival and gross outcome, and performs more poorly in predicting later and more detailed functional outcomes, particularly in cognitive and emotional realms.121 The Center for Disease Control provides the following guidelines for the Glasgow Coma Scale. Medical responders should use the scale to assess the level of severity of brain injury.98

Glasgow Coma Scale Eye Opening Response • Spontaneous--open with blinking at baseline 4 points • To verbal stimuli, command, speech 3 points • To pain only (not applied to face) 2 points • No response 1 point

Verbal Response • Oriented 5 points • Confused conversation, but able to answer questions 4 points • Inappropriate words 3 points • Incomprehensible speech 2 points • No response 1 point

Motor Response • Obeys commands for movement 6 points • Purposeful movement to painful stimulus 5 points • Withdraws in response to pain 4 points • Flexion in response to pain (decorticate posturing) 3 points • Extension response in response to pain (decerebrate posturing) 2 points • No response 1 point

Categorization: Coma • No eye opening, no ability to follow commands, no word verbalizations (3-8)

Head Injury Classification • Severe Head Injury----GCS score of 8 or less • Moderate Head Injury----GCS score of 9 to 12 • Mild Head Injury----GCS score of 13 to 15)

11 nursece4less.com nursece4less.com nursece4less.com nursece4less.com After the Glasgow Coma Scale is administered, further testing is conducted to determine the level of damage and the severity of the injury. Imaging tests are used to assist with the diagnosis of the patient as well as to make a determination about the prognosis of the patient.28 Skull and neck X-rays are used to check for bone fractures and spinal instability in patients with mild to moderate injuries.122 In patients with mild head injuries, a diffusion tensor imaging is sometimes used. This device can reliably detect and track brain abnormalities and is sensitive enough to be used on patients with mild injury.71 In some cases, a magnetoencephalography may be used to obtain further information regarding a mild case of head trauma.62

Additional diagnostic imaging is used in cases of moderate to severe head injury. In these instances, patients will be assessed using a CT scan. This scan creates cross sectional X-ray images of the head and brain and is used to identify any bone fractures that might be present in the skull. The CT scan also indicates if there is the presence of hemorrhage, hematomas, contusions, brain tissue swelling, and tumors.123

Once the initial assessment is complete, additional imaging may be conducted. In these instances, a magnetic resonance imaging (MRI) is often used to determine if there is additional damage beyond the scope of the initial assessment. The MRI is used to determine if there have been any subtle changes in the brain tissue and are used when more detail is needed than standard X-rays can provide.17 MRI’s are not used during the initial emergency assessment as they require a significant amount of time and are not always available during the initial assessment.6 However, an MRI is an important diagnostic tool and should be used when appropriate and available.

12 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Examination

When a patient is evaluated to have a head injury, he or she will undergo a complete examination with the purpose of assessing the trauma and identifying specific injuries. While the examination will vary depending on the patient’s needs, there are standard examination methods that are typically used during the initial examination. Regardless of the type of injury (blunt or penetrating, open or closed) the initial examination will be conducted as soon as possible and will often occur in conjunction with .124 It is important to conduct the initial assessment as soon as possible to identify any life-threatening injuries and to minimize any additional damage. Early identification of any complications will reduce the likelihood of the patient developing secondary injuries.104

While it is important to manage any damage caused by an open head , it should not interfere with the initial stabilization of the patient. Therefore, the initial stage of the patient examination will include assessing and managing the airway, breathing, circulation, and related components.34 Once that is complete, the emergency clinician will begin the primary survey. The primary examination will focus on identifying any complications or secondary injuries.125 The following guidelines are provided for the primary and secondary examination of the patient.

Primary Examination

As part of the primary survey, the pupillary size and reactions are noted and the conscious state is assessed. Disturbances of consciousness may follow focal damage to the reticular formation, which extends from the rostral midbrain to the caudal medulla. It receives input from all sensory pathways and projects widely to the cerebral cortex and limbic system. Focal cortical lesions do not affect consciousness, but coma may result from general depression of the cerebral cortex.

Using purely descriptive methods to assess conscious state is problematic.

13 nursece4less.com nursece4less.com nursece4less.com nursece4less.com One observer’s “somnolent” is another’s “drowsy.” When is a person stuporous and when are they obtunded? What is semi-conscious and when does a clouded conscious state become coma? Consciousness is a continuum and clinicians use the Glasgow Coma Scale (GCS) as a measure (albeit crude) of level of consciousness.

Secondary Examination

Once the primary survey is complete, the secondary survey should include a more thorough neurological examination, starting with a reassessment of the Glasgow Coma Scale, and an examination of the head, face and neck. The head and face should be examined for lacerations and fractures. Scalp lacerations can be palpated with a gloved finger. If there is an underlying depressed fracture, surgery will be required. Profuse bleeding may occur from a scalp laceration and this can be controlled with a pressure dressing or by a few temporary full-thickness sutures.

The nose and are inspected for leaks of cerebrospinal fluid (CSF). This is usually mixed with blood and results in a thinner discharge that will separate on blotting paper. If this is not available, the separation can also be observed on a sheet or pillowcase. If there is CSF rhinorrhea or otorrhoea, a basal is present (regardless of whether it can be seen on radiographs). Bilateral periorbital hematomas (raccoon eyes) and subconjunctival hemorrhages where the posterior margin cannot be seen are both indicators of anterior fossa fracture. Hemotympanum or bruising over the mastoid (Battle’s sign) suggests a middle fossa fracture. Battle’s sign usually takes several hours to develop. The nose, mid face and orbits should also be palpated for fractures that may require treatment later. When the patient is log-rolled, the back of the head and cervical spine should also be examined.

The neurological examination will be limited because of the lack of cooperation of the patient, but it should still be possible at least to determine if there are lateralizing signs such as a hemiparesis or a third cranial nerve palsy. Higher functions are assessed first. Most often this will be limited to level of consciousness and, in particular, the “voice” component of the GCS. In a relatively cooperative patient with a focal injury it may be possible to assess language further, but in the early period after a head injury it will be difficult to differentiate dysphasia from confusion. Memory becomes important later and the period of post-traumatic amnesia is used as an indicator of injury severity.

Cranial Nerves: Many of the cranial nerves can be assessed even in the unconscious patient.

I (olfactory): Assessment obviously requires cooperation, but this nerve should be examined when possible, as it is the most commonly affected cranial nerve after head injury and is often ignored. Anosmia may seem trivial but it has significant effects beyond enjoyment of food and wine. Anosmic patients will not be able to smell smoke from a fire or leaking gas, both of which may potentially put them at risk.

14 nursece4less.com nursece4less.com nursece4less.com nursece4less.com II (optic): The pupillary reactions to light depend on the integrity of the optic and oculomotor nerves, as well as their connections. Normally both pupils should constrict when light is shone in either eye or when the patient looks at a near object (accommodation reflex). A pupil that responds to direct light implies that the ipsilateral optic and oculomotor nerves are intact. If it responds to direct light, but not consensually, this implies damage to the contralateral optic nerve. A pupil reacting only consensually suggests ipsilateral optic nerve damage. An oculomotor will produce an ipsilateral dilated pupil, which does not respond directly or consensually, but the contralateral pupil will constrict when light is shone in either eye.

One must remain aware that the commonest cause of a dilated pupil after head injury is traumatic due to local ocular trauma. This should be suspected if the dilated pupil was present right from the time of injury and there is local trauma to the globe or orbit.

During examination of the eyes the fundi are assessed. One would not expect to see papilledema in the early hours after a head injury, and funduscopy is done more for the purpose of assessing the integrity of the eye itself (checking for retinal detachment or hemorrhage, vitreous hemorrhage, corneal laceration, etc.). Contact lenses should be looked for and removed. Visual fields can be checked by confrontation in a cooperative patient or by menace in an uncooperative patient. They are not clinically assessable in the unconscious patient.

III, IV and VI (oculomotor, trochlear and abducens): The pupils are assessed as above. Ptosis (III) is difficult to assess in patients who are unconscious. Ocular movements can be observed and any dysconjugate movements noted. If the patient is cooperative this is easy. An alert but uncooperative patient can be made to look at objects quite readily by placing them in their field of vision. This also applies to children.

Oculocephalic reflexes test the third, fourth and sixth cranial nerves and their connections. Movement of the head from side to side or up and down will be accompanied by movement of the eyes in the opposite direction, resulting in a constant point of fixation.

The term “doll’s eyes” is often used to describe oculocephalic reflexes but this frequently leads to confusion. Whether doll’s eyes are normal or abnormal depends on the sophistication of the doll. One with eyes painted on would describe the abnormal and one with eyes free to rotate would better approximate the normal situation.

It is preferable to avoid the term altogether and describe oculocephalic reflexes as being normal or abnormal. It is not usually recommended to test oculocephalic reflexes in a head-injured patient owing to the high risk of associated cervical spinal injury. If it is important to know if these reflexes are intact (i.e., in assessing brain death), caloric testing is usually undertaken.

15 nursece4less.com nursece4less.com nursece4less.com nursece4less.com V (trigeminal): The motor component of the trigeminal nerve can be tested in a cooperative patient, but the sensory part can be assessed even in the unconscious. Painful stimuli applied to the supraorbital nerve should usually produce a response and the corneal reflex tests trigeminal function as well as facial nerve function.

VII (facial): Facial movements are readily assessed in the cooperative patient, but can also be observed when painful stimuli are applied and as part of the corneal reflex. Facial nerve palsies are often seen with middle fossa fractures and this nerve should be assessed early in any patient with CSF otorrhoea or Battle’s sign. Taste is not usually tested. Patients often complain of loss of taste after a head injury but this is usually due to anosmia.

VIII (acoustic): This is hard to test clinically in the unconscious patient. An alert but uncooperative patient can be observed for reaction to sudden noises. Assessment in the unconscious usually requires brainstem auditory evoked potential monitoring. This nerve is also often injured in middle fossa fractures.

IX (glossopharyngeal), X (vagus): There is usually little more to do than observe swallowing and test the gag reflex, either directly or by moving an endotracheal tube.

XI (accessory): Sternomastoid and trapezius function can be tested, but it is unusual for the accessory nerve to be injured intracranially.

XII (hypoglossal): A hypoglossal nerve injury will force the protruded tongue to the ipsilateral side. Over time the ipsilateral side of the tongue becomes wasted.

Motor Function: The sophistication of motor testing depends on the level of cooperation of the patient. At the least, it is possible to detect asymmetry in movement or responses to pain as described above in assessing the GCS. Reflexes are often brisk but may be absent with associated (spinal ). Plantar reflexes will usually be extensor after a significant head injury. Priapism and loss of anal tone are other indicators of spinal cord injury that should be sought.

Sensory Function: The same applies as for motor function. If there is a response to pain, this can be compared in different areas. This is important when a spinal cord injury is suspected and one is attempting to determine at what level. Sometimes there can be movement of limbs through local spinal cord reflexes; hence, when assessing a patient for brain death, it is mandatory that the painful stimulus is applied to a cranial nerve distribution.

16 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Traumatic Brain Injury Assessment

If traumatic brain injury is suspected, the patient will undergo a more thorough examination, which will include the following assessments.126

Cognitive • Orientation • Command following (single, multistep) • Attention • Concentration • Memory (short- and long-term) • Naming/repetition • Abstract thinking • Judgment

Behavioral • Depression • Anxiety • Irritability • Agitation • Restlessness • Disinhibition

Musculoskeletal • Manual muscle (strength) testing • Joint range of motion (including temporomandibular joint) • Muscle tone • Mobility • Balance — sitting, standing, dynamic • Transfers • Gait — indoor, outdoor, stair

17 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Neurologic

§ Cranial nerve testing

§ Sensory function

§ Special sensory - Vision - Hearing - Smell/taste

§ Deep tendon reflexes

§ Primitive reflexes (frontal release signs) - Palmomental reflex - Snout reflex - Glabellar (tap) reflex - Palmar grasp reflex

§ Brainstem reflexes - Oculocardiac reflex - Horizontal oculocephalic/oculovestibular reflex - Pupillary light reflex - Vertical oculocephalic/oculovestibular reflex - Fronto-orbicular reflex

§ Bowel/bladder reflexes - Cremasteric reflex - Bulbocavernosus reflex - Anal wink reflex

§ Cerebellar testing - Finger to nose (upper extremity dysmetria) - Heel to shin (lower extremity dysmetria)

§ Fine and gross motor coordination (tremor)

§ Autonomic

18 nursece4less.com nursece4less.com nursece4less.com nursece4less.com General Medical Exam

§ Skin

§ Heart/circulation

§ Lung

§ Abdomen - Digestive - Bowel

§ Genitourinary

§ Endocrine

Radiologic Imaging

In many instances, the examination will include radiologic imaging.

Prevention and Treatment of Intracranial Hypertension

In normal individuals with closed cranial fontanelles, central nervous system contents, including brain, spinal cord, blood, and cerebrospinal fluid (CSF), are encased in a noncompliant skull and vertebral canal, constituting a nearly incompressible system. There is a small amount of capacitance in the system provided by the intervertebral spaces. In the average adult, the skull encloses a total volume of 1450 mL: 1300 mL of brain, 65 mL of CSF, and 110 mL of blood. The Monroe-Kellie hypothesis states the sum of the intracranial volumes of blood, brain, CSF, and other components is constant, and that an increase in any one of these must be offset by an equal decrease in another, or else pressure increases. An increase in pressure caused by an expanding intracranial volume is distributed evenly throughout the intracranial cavity.

The normal range for ICP varies with age. Values for pediatric subjects are not as well established. Normal values are less than 10 to 15 mmHg for

19 nursece4less.com nursece4less.com nursece4less.com nursece4less.com adults and older children, 3 to 7 mmHg for young children, and 1.5 to 6 mmHg for term infants. Intracranial pressure can be subatmospheric in newborns. Normal adult ICP is defined as 5 to 15 mm Hg (7.5–20 cm H2O). ICP values of 20 to 30 mm Hg represent mild intracranial hypertension; however, when a temporal mass lesion is present, herniation can occur with ICP values less than 20 mmHg. Intracranial pressure values greater than 20 to 25 mmHg require treatment in most circumstances. Sustained ICP values of greater than 40 mmHg indicate severe, life-threatening intracranial hypertension.127,128

Special features should be considered in patients with traumatic brain injury (TBI), in which lesions may be heterogeneous, and several factors often contribute to increase the ICP:24 1. Traumatically induced masses: epidural or subdural hematomas, hemorrhagic contusions, foreign body, and depressed skull fractures 2. 3. Hyperemia owing to vasomotor paralysis or loss of autoregulation 4. Hypoventilation that leads to hypercarbia with subsequent cerebral vasodilation 5. Hydrocephalus resulting from obstruction of the CSF pathways or its absorption 6. Increased intrathoracic or intraabdominal pressure as a result of mechanical ventilation, posturing, agitation, or Valsalva maneuvers

After evacuation of traumatic mass lesions, the most important cause of increased ICP was thought to be vascular engorgement. Recent studies have suggested that cerebral edema is the primary cause in most cases.

20 nursece4less.com nursece4less.com nursece4less.com nursece4less.com A secondary increase in the ICP often is observed 3 to 10 days after the trauma, principally as a result of a delayed hematoma formation, such as epidural hematomas, acute , and traumatic hemorrhagic contusions with surrounding edema, sometimes requiring evacuation. Other potential causes of delayed increases in ICP are cerebral , hypoventilation, and hyponatremia.117

Intracranial hypertension is an important cause of secondary injury in patients with acute neurologic and neurosurgical disorders and typically mandates specific monitoring. Patients with suspected intracranial hypertension, especially secondary to TBI, should have monitoring of ICP; monitoring of cerebral oxygen extraction, as with jugular bulb oximetry or brain tissue PO2, may also be indicated. Brain-injured patients also should have close monitoring of systemic parameters, including ventilation, oxygenation, electrocardiogram, heart rate, blood pressure, temperature, blood glucose, and fluid intake and output. Patients should be monitored routinely with pulse oximetry and capnography to avoid unrecognized hypoxemia and hypoventilation or hyperventilation. A central venous catheter commonly is needed to help evaluate volume status, and a Foley catheter is employed for accurate urine output.129

Clinical symptoms of increased ICP, such as headache, nausea, and vomiting, are impossible to elicit in comatose patients. Papilledema is a reliable sign of intracranial hypertension, but is uncommon after head injury, even in patients with documented elevated ICP. In a study of patients with head trauma, 54% of patients had increased ICP, but only 3.5% had papilledema on fundoscopic examination. Other signs, such as pupillary dilation and decerebrate posturing, can occur in the absence of intracranial hypertension. CT scan signs of brain swelling, such as midline shift and

21 nursece4less.com nursece4less.com nursece4less.com nursece4less.com compressed basal cisterns, are predictive of increased ICP, but intracranial hypertension can occur without those findings.28,81

The ventriculostomy catheter is the preferred device for monitoring ICP and the standard against which all newer monitors are compared. An intraventricular catheter is connected to an external pressure transducer via fluid-filled tubing. The advantages of the ventriculostomy are its relatively low cost, the option to use it for therapeutic CSF drainage, and its ability to recalibrate to minimize errors owing to measurement drift. The disadvantages are difficulties with insertion into compressed or displaced ventricles, inaccuracies of the pressure measurements because of obstruction of the fluid column, and the need to maintain the transducer at a fixed reference point relative to the patient’s head. The system should be checked for proper functioning at least every 2 to 4 hours, and any time there is a change in the ICP, neurologic examination, and CSF output. This check should include assessing for the presence of an adequate waveform, which should have respiratory variations and transmitted pulse pressure.78

When the ventricle cannot be cannulated, other alternatives can be used. Different non–fluid-coupled devices are available for ICP monitoring and have replaced the subarachnoid bolt. The microsensor transducer and the fiberoptic transducer are the most widely available. These transducer-tipped catheters can be inserted in the subdural space or directly into the brain tissue. The main advantages of these monitors are the ease of insertion, especially in patients with compressed ventricles; however, none of the transducer-tipped catheters can be reset to zero after they are inserted into the skull, and they exhibit measurement drift over time. Subdural and epidural monitors for ICP measurements are less accurate compared to ventriculostomy or parenchymal monitors.65

22 nursece4less.com nursece4less.com nursece4less.com nursece4less.com For surgical patients, the ICP monitor may be inserted at the end of the surgical procedure. Intracranial pressure monitoring is continued for as long as treatment of intracranial hypertension is required, typically 3 to 5 days. A secondary increase in ICP may be observed 3 to 10 days after trauma in 30% of patients with intracranial hypertension secondary to development of delayed intracerebral hematoma, cerebral vasospasm, or systemic factors such as hypoxia and .18

The variations seen in the normal tracing of ICP originate from small pulsations transmitted from the systemic blood pressure to the intracranial cavity. These blood pressure pulsations are superimposed on slower oscillation caused by the respiratory cycle. In mechanically ventilated patients, the pressure in the superior vena cava increases during inspiration, which reduces venous outflow from the cranium, causing an elevation in ICP.38

As the ICP increases, cerebral compliance decreases, arterial pulses become more pronounced, and venous components disappear. Pathologic waveforms include Lundberg A, B, and C types. Lundberg A waves or plateau waves are ICP elevations to more than 50 mmHg lasting 5 to 20 minutes. These waves are accompanied by a simultaneous increase in MAP, but it is not clearly understood if the change in MAP is cause or effect. Lundberg B waves or pressure pulses have an amplitude of 50 mmHg and occur every 30 seconds to 2 minutes. Lundberg C waves have an amplitude of 20 mmHg and a frequency of 4 to 8 per minute; they are seen in the normal ICP waveform, but high-amplitude C waves may be superimposed on plateau waves.130

Monitoring of ICP is an invasive technique and has some associated risks. For a favorable risk-to-benefit ratio, ICP monitoring is indicated only in

23 nursece4less.com nursece4less.com nursece4less.com nursece4less.com patients with significant risk of intracranial hypertension. Patients with TBI who are particularly at risk for developing an elevated ICP include those with Glasgow Coma Scale of 8 or less after cardiopulmonary resuscitation and who have an abnormal admission head CT scan. Such abnormalities might include low-density or high-density lesions, including contusions, epidural, subdural, or intraparenchymal hematomas, compression of basal cisterns, and edema. Patients who are able to follow commands have a low risk for developing intracranial hypertension, and serial neurologic examinations can be followed.91

Although CT scan findings are not accurate in determining the actual ICP, the risk of developing intracranial hypertension can be predicted. Sixty percent of patients with closed head injury and an abnormal CT scan have intracranial hypertension. Only 13% of patients with a normal CT scan have elevated ICP except for patients with certain risk factors, including age greater than 40 years old, systolic blood pressure less than 90 mmHg, and decerebrate or decorticate posturing on motor examination.

Patients with a normal CT scan have 60% risk of intracranial hypertension if they have two risk factors and 4% if they have only one risk factor. Patients with a Glasgow Coma Scale score greater than 8 also might be considered for ICP monitoring if they require treatment that would not allow serial neurologic examinations, such as prolonged anesthesia for surgery of multiple injuries or prolonged pharmacologic paralysis for ventilatory management, or if they require a treatment that might increase ICP, such as positive end-expiratory pressure (PEEP). Other, less common indications include patients with multiple systemic injuries with altered level of consciousness and subsequent to removal of an intracranial mass (i.e., hematoma, tumor). Intracranial pressure monitoring also must be

24 nursece4less.com nursece4less.com nursece4less.com nursece4less.com considered in nontraumatic conditions in which an intracranial mass lesion is present (i.e., cerebral infarction, spontaneous ) and has a likelihood of expansion leading to intracranial hypertension and clinical deterioration. The duration of monitoring is until ICP has been normal for 24 to 48 hours without ICP .59,131

Prevention or treatment of factors that may aggravate or precipitate intracranial hypertension is a cornerstone of neurologic critical care. Specific factors that may aggravate intracranial hypertension include obstruction of venous return (head position, agitation), respiratory problems (airway obstruction, hypoxia, hypercapnia), fever, severe hypertension, hyponatremia, anemia, and seizures.29

Effective treatment of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased ICP. When ICP becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. Medical management of increased ICP should include sedation, drainage of CSF, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension, refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from TBI.11,132

Neuromonitoring In Critical Care Management

During neurointensive care of patients with severe traumatic brain injuries, general parameters that are regularly monitored include electrocardiography

(ECG) monitoring, arterial oxygen saturation (pulse oximetry or SpO2), capnography (end-tidal CO2, PetCO2), arterial blood pressure (arterial

25 nursece4less.com nursece4less.com nursece4less.com nursece4less.com catheter), central venous pressure (CVP), systemic temperature, urine output, arterial blood gases, and serum electrolytes and osmolality. Invasive or non-invasive cardiac output monitoring may be required in hemodynamically unstable patients who do not respond to fluid resuscitation and vasopressors.

Prior to arrival to the ICU, patients with severe TBI are usually received, resuscitated and stabilized in emergency department or operating room. Once the severely head-injured patient has been transferred to the ICU, the management consists of the provision of high quality general care and various strategies aimed at maintaining hemostasis with 1) stabilization of the patient, if still unstable, 2) prevention of intracranial hypertension, 3) maintenance of an adequate and stable cerebral pressure (CPP), 4) avoidance of systemic, secondary brain insults (SBI), and 5) optimization of cerebral hemodynamic and oxygenation.

Monitoring of patients with severe TBI is essential for the guidance and optimization of therapy. The rationale of monitoring is early detection and diagnosis of secondary brain insults, both systemic and intracranial. Therefore, monitoring of patients with severe TBI must comprise both general and specific neurologic monitoring. Management of a patient with a head injury will differ depending on severity. To ensure consistency with patient care, a standard set of guidelines for the management of head injuries has been developed. These guidelines provide critical care recommendations for the patient. The specific strategies used will depend on the patient’s specific needs. The table below provides an overview of the different types of interventions for patients with head injuries.11,16,33,35,45,66,72,104,105,107,113,132-138

Multidisciplinary Care A coordinated, multidisciplinary healthcare team should

26 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Team be established at the time of the patient’s admission and implemented for the duration of hospitalization. It should include one or more (such as trauma surgeons, intensivists, and neurosurgeons), nurses, respiratory therapists, pharmacists, nutritionists, physical therapists, occupational therapists, speech language pathologists, physiatrists, case managers, social workers, and clergy. The patient’s family should be involved as well.

Blood Pressure and An arterial catheter should be inserted to monitor blood Volume Management pressure and allow frequent blood sampling. During the acute post-injury phase, hypotension should be avoided; if it occurs, the patient’s volume status should be evaluated first and hypotension should be corrected rapidly.

A urinary catheter is inserted to assess adequacy of renal perfusion. The kidney requires 20% to 25% of cardiac output; commonly, it’s the first organ to show the effects of impaired perfusion or intravascular volume. Multiple intravenous (IV) access sites should be established; at least one of these sites for central venous catheter (CVC), which allows fluid and drug administration, and CVC monitoring to assess volume status. If volume status is inadequate, the patient should receive additional IV fluids. For persistent hypotension, continuous infusion of a vasoactive drug (such as dopamine or norepinephrine) should begin once adequate intravascular volume is restored.

As the patient’s volume and blood pressure status stabilize and intracranial hypertension resolves, the need for aggressive volume management and vasoactive drugs decreases. To minimize the risk of bloodstream infection, invasive vascular devices (such as a CVC and arterial line) should be removed as soon as the patient stabilizes.

Brain and tissue Low peripheral oxygen saturation values or low arterial oxygenation blood oxygen values (as shown by arterial blood gas testing) should be avoided. Maintaining adequate brain tissue oxygenation seems to improve patient outcomes. However, systemic oxygen levels don’t always accurately represent the brain’s oxygen level; to assess this level directly, a special catheter may be inserted into the brain or jugular vein. If such a device is used, oxygen administration can be adjusted accordingly.

Many TBI patients require prolonged mechanical ventilation and may benefit from a tracheotomy. A tracheotomy helps reduce the risk of ventilator- associated pneumonia (VAP), as do suctioning of

27 nursece4less.com nursece4less.com nursece4less.com nursece4less.com secretions above the tracheotomy cuff, maintaining the head of the bed at 30 degrees, and performing good oral care every 4 hours.

Both jugular venous oxygen saturation (SjvO2) and brain tissue oxygen tension (PbtO2) monitoring measure cerebral oxygenation, however,

SjvO2 measures global cerebral oxygenation and PbtO2 measures focal cerebral oxygenation using an invasive probe. Rosenthal, et al., documented that, measurements of PbtO2 represent the product of cerebral blood flow (CBF) and the cerebral arteriovenous oxygen tension difference rather than a direct measurement of total oxygen delivery or cerebral oxygen.

PbtO2 is the most reliable technique to monitor focal cerebral oxygenation in order to prevent episodes of desatuartion. However, global cerebral oxygenation alterations may not be observed. The normal

PbtO2 ranges between 35 mmHg and 50 mmHg. A value of a PbtO2 < 15 mmHg is considered a threshold for focal cerebral and treatment. Several studies

demonstrated that PbtO2-based therapy may be associated with reduced patient mortality and improved patient outcome after severe TBI.

Ventilation The patient’s arterial carbon dioxide (CO2) value should be maintained in the low-normal range. A very low CO2 level can contribute to vasoconstriction, which in turn may decrease cerebral blood flow. As intracranial hypertension resolves, the CO2 level can be allowed to return to the normal range.

Clinical care includes continual monitoring for hypoventilation (as shown by diminished breath sounds and somnolence increased from baseline) and assisted secretion removal.

Osmotherapy Osmotherapy aims to increase the osmolality of the intravascular space, which in turn helps mobilize excess fluid from brain tissue. If intracranial pressure increases, mannitol (an osmotic diuretic) may be given to decrease cerebral edema, transiently increase intravascular volume, and improve cerebral blood flow. Hypertonic saline solution (saline concentrations of 3% to 24%) may be used to promote osmotic mobilization of water across the blood-brain barrier.

28 nursece4less.com nursece4less.com nursece4less.com nursece4less.com ICP Monitoring Intracranial pressure should be monitored in all salvageable patients with severe TBI and an abnormal computed tomography (CT) scan. Also, ICP monitoring is indicated in patients with severe TBI with a normal CT scan for factors of age (i.e., over 40 years), unilateral or bilateral motor posturing, or systolic blood pressure hypotension, i.e., < 90 mmHg. Based on physiological principles, potential benefits of ICP monitoring include earlier detection of intracranial mass lesion, guidance of therapy and avoidance of indiscriminate use of to control ICP, drainage of cerebrospinal fluid (CSF) with reduction of ICP and improvement of cerebral perfusion pressure (CPP), and determination of prognosis.

Currently, available methods for ICP monitoring include epidural, subdural, subarachnoid, parenchymal, and ventricular locations. Historically, ventricular ICP catheter has been used as the reference standard and the preferred technique when possible. As the most accurate, low-cost, and reliable method of trending pressure intracranially, ICP monitoring also allows for continuous measurement of ICP and for therapeutic CSF drainage in the event of intracranial hypertension to control raised pressures. Subarachnoid, subdural, and epidural monitors are less accurate.

ICP monitoring is usually placed via the right side, since in approximately 80% of the populations the right hemisphere is the non-dominant, unless contraindicated. However, it might be placed on the side with maximal pathological features or swelling. Routine ventricular catheter change or prophylactic use for ventricular catheter placement is not recommended to reduce infection. ICP monitoring devices are usually continued for ≤1 week; with daily examination of the CSF for glucose, protein, cell count, Gram stain, and culture and sensitivity.

Treatment for intracranial hypertension should be started with ICP thresholds above 20 mmHg. Additional to ICP values, clinical and brain CT findings should be used to determine the need for treatment.

To aid rapid identification of increased ICP, a monitoring device may be inserted through a small hole drilled into the skull. Parenchymal, epidural, subdural, and subarachnoid monitoring devices can be used. In some cases, an extraventricular drain (ventriculostomy) may be placed.

When caring for patients with any of these devices,

29 nursece4less.com nursece4less.com nursece4less.com nursece4less.com aseptic standards should be followed. CSF characteristics (including cloudiness and volume changes) should be monitored to help detect infection early. Routine care should be performed for the insertion site. Entry into the drainage system should be minimized and such safety precautions as restricting changes in head-of-bed elevation and securing the extraventricular drain to prevent dislodgment should be maintained.

Jugular bulb venous The jugular venous oxygen saturation (SjvO2) is an oxygen saturation indicator of both cerebral oxygenation and cerebral metabolism, reflecting the ratio between cerebral blood flow (CBF) and cerebral metabolic rate of oxygen

(CMRO2). A retrograde catheterization of the internal jugular vein (IJV) is used for SjvO2 monitoring. As the right IJV is usually dominant, it is commonly used for cannulation to reflect the global cerebral oxygenation.

Monitoring SjvO2 can be either continuous via a fiberoptic catheter or intermittent via repeated blood samples. In a prospective study of patients with severe acute brain trauma and intracranial hypertension, continuous monitoring of SjvO2 has been associated with improved outcome. The normal average of the

SjvO2, in a normal awake subject, is 62% with a range of 55% to 71%.

A sustained jugular venous desaturation of < 50% is the threshold of cerebral ischemia and for treatment. SjvO2 monitoring can detect clinically occult episodes of cerebral ischemia, allowing the prevention of these

episodes by simple adjustment of treatment.

In TBI, jugular venous desaturation is mostly related to CBF reduction secondary to decreased CPP (hypotension, intracranial hypertension, and vasospasm) or hypocapnia-associated cerebral vasoconstriction. Studies showed that a sustained reduction of the SjvO2 < 50% was associated with poor outcome, and an independent risk factor for poor prognosis. Consequently, SjvO2 monitoring is essential for adjustment of ventilation during the medical treatment of an established intracranial hypertension. The benefit of SjvO2 monitoring on severe TBI patients' outcomes has not been confirmed in study trials.

CPP Monitoring Cerebral ischemia is considered the single most important secondary event affecting outcome following severe TBI. CPP below 50 mmHg should be avoided. A low CPP may jeopardize regions of the brain with pre- existing ischemia, and enhancement of CPP may help to avoid cerebral ischemia. The CPP value to target should

30 nursece4less.com nursece4less.com nursece4less.com nursece4less.com be maintained above the ischemic threshold at a minimum of 60 mmHg.

Maintenance of a CPP greater than 60 mmHg is a therapeutic option that may be associated with a substantial reduction in mortality and improvement in quality of survival, and is likely to enhance perfusion to ischemic regions of the brain following severe TBI.

There is no evidence that the incidence of intracranial hypertension, morbidity, or mortality is increased by the active maintenance of CPP above 60 mmHg with normalizing the intravascular volume or inducing systemic hypertension. Both 60 mmHg and 70 mmHg are cited in the literature as the threshold above which CPP should be maintained.

The CPP should be maintained at a minimum of 60 mmHg in the absence of cerebral ischemia, and at a minimum of 70 mmHg in the presence of cerebral

ischemia. PbtO2 monitoring has been suggested to identify individual optimal CPP. In the absence of cerebral ischemia, aggressive attempts to maintain CPP above 70 mmHg with fluids and vasopressors should be avoided because of the risk of acute respiratory distress syndrome (ARDS).

Cerebral perfusion pressure (CPP) should be maintained at an appropriate level by optimizing volume status, as with IV fluids, osmotherapy, and vasoactive drugs. A brain tissue oxygen monitor may be used to help determine which CPP and ICP levels the

patient tolerates best.

Cerebral Microdialysis Cerebral microdialysis (MD) is a recently developed invasive laboratory device, bedside monitor to analyze brain tissue biochemistry. Usually, a MD catheter is inserted in "susceptible" brain tissue to measure biochemical changes in the area of brain most vulnerable to secondary insults. Different assays are available to measure dialysate concentrations including glucose, lactate, pyruvate, glycerol, and glutamate.

Typically, cerebral hypoxia or ischemia results in a significant increase in the lactate: pyruvate ratio (LPR). A LPR > 20-25 is considered a threshold for cerebral ischemia and is associated with poor outcome in TBI. Although, MD is a well-established tool that provides additional assistance in the management of patients with severe TBI, its use is very limited.

Transcranial Doppler (TCD) is a non-invasive method to Ultrasonography measure CBF velocity. It is increasingly utilized in

31 nursece4less.com nursece4less.com nursece4less.com nursece4less.com neurocritical care including TBI. TCD is a clinically useful tool in the diagnosis of complications that may occur in patients with TBI such as vasospasm, critical elevations of ICP and decreases in CPP, carotid dissection, and cerebral circulatory arrest (brain death). TCD can predict post-traumatic vasospasm prior to its clinical manifestations.

Since ICP monitoring is an invasive procedure with potential risk of associated complications, TCD has been suggested as a non-invasive alternative technique for assessment of ICP and CPP. The overall sensitivity of TCD for confirming brain death is 75% to 88%, and the overall specificity is 98%. Although, TCD is an established monitoring modality in neurocritical care, evidence to support its regular use for ICP/CPP management in severe TBI patients is lacking.

Electroencephalogram Electroencephalogram (EEG) is a clinically useful tool Monitoring for monitoring the depth of coma, detecting non- convulsive (sub-clinical) seizures or seizures activity in pharmacologically paralyzed patients, and diagnosing brain death. Continuous EEG has been suggested for the diagnosis of post-traumatic seizures (PTS) in patients with TBI, especially in those who are receiving neuromuscular blockades.

Sensory-evoked potentials (SEP) can yield data on current brain function in very severe TBI patients; however, their use is very limited in the initial management of TBI.

Near Infrared Near infrared spectroscopy (NIRS) is a continuous, Spectroscopy direct, and non-invasive monitor of cerebral oxygenation and cerebral blood volume (CBV). In cerebral tissue, the two main chromophores (light- absorbing compounds) are hemoglobin (Hb) and cytochrome oxidase. NIRS is based on the differential absorption properties of these chromophores in the NIR range, i.e., between 700 and 1,000 nm. At 760 nm, Hb occurs primarily in the deoxygenated state (deoxyHb), whereas at 850 nm, it occurs in the oxygenated state (oxyHb). Hence, by monitoring the difference in absorbency between these two wavelengths, the degree of tissue deoxygenation can be evaluated.

In comparison with the SjvO2, NIRS is less accurate in determining cerebral oxygenation. Although, NIRS is an evolving technology and a potential as a clinical tool for bedside cerebral oxygenation and CBF measurements, its use in neurocritical care remains very limited. Anesthetic, Sedative, In severe TBI patients, endotracheal intubation, and Analgesic Agents mechanical ventilation, trauma, surgical interventions

32 nursece4less.com nursece4less.com nursece4less.com nursece4less.com (if any), nursing care and ICU procedures are potential causes of pain.

Narcotics, such as morphine, fentanyl and remifentanil, should be considered first line therapy since they provide analgesia, mild sedation and depression of airway reflexes (cough) which all required in intubated and mechanically ventilated patients.

Administration of narcotics is either as continuous infusions or as intermittent boluses. Adequate sedation potentiates analgesics, provides anxiolysis, limits elevations of ICP related to agitation, discomfort, cough or pain, facilitates nursing care and mechanical

ventilation, decrease O2 consumption and CO2 Production, improves patient comfort, and prevents harmful movements.

The ideal sedative for TBI patient would be rapid in onset and offset, easily titrated to effect, and lack active metabolites. It would be anticonvulsant, able to lower ICP, and to preserve the neurologic examination. Finally, it would lack deleterious cardiovascular effects.

No commonly used sedative is ideal. Propofol is the hypnotic of choice in patients with an acute neurologic insult, as it is easily titratable and rapidly reversible once discontinued. These properties permit predictable sedation yet allow for periodic neurologic evaluation of the patient. Propofol should be avoided in hypotensive or hypovolemic patients because of its deleterious hemodynamic effects. Moreover, propofol infusion syndrome (, metabolic acidosis, renal failure, and bradycardia) is a potential complication of prolonged infusions or high doses of propofol administration.

Benzodiazepines such as midazolam and lorazepam are recommended as continuous infusion or intermittent boluses. In addition to sedation, they provide amnesia and anticonvulsive effect. Prolonged infusion, high dose, presence of renal or hepatic failure, and old age are risk factors for accumulation and oversedation.

Short-acting anesthetic and sedative-analgesic agents, such as propofol and fentanyl, typically are given. When dosages are decreased, the patient can be awakened quickly, permitting non-pharmacologically tainted assessment of neurologic status.

When explaining “wake-up” assessment to family members, the clinician should inform them that the patient doesn’t actually wake up and return to a pre-

33 nursece4less.com nursece4less.com nursece4less.com nursece4less.com injury condition. As the patient improves, dosages are reduced gradually. The patient must be monitored for pain; if needed, enterally administered analgesia should be considered to manage pain without causing significant neurologic status changes.

Pentobarbital may be given to control increased ICP in patients who don’t respond to first-line therapies. Called pentobarbital coma, this approach minimizes the brain’s electrical activity for several days. The exact mechanism of pentobarbital coma isn’t known. Routine use of neuromuscular blocking agents (NMBAs) to paralyze patients with TBI is not recommended. NMBAs reduce elevated ICP and should be considered as second line therapy for refractory intracranial hypertension. However, the use of a NMBA is associated with increased risk of pneumonia and ICU length of stay (LOS), and with neuromuscular complications.

Temperature The damaged brain is more susceptible to increased Management temperature, so the patient should be kept normothermic (typically at 95° to 98.6° F [35° to 37° C]) to reduce brain metabolism and promote anti- inflammatory effects. Cooled water or saline solution circulated through external body wraps or special intravascular cooling catheters can be used to maintain the desired temperature. Although ice packs may be used, they are labor intensive and may lead to inconsistent cooling.

Once intracranial hypertension resolves, the patient’s temperature can be allowed to normalize. Moderate systemic hypothermia at 32°C to 34°C, reduces cerebral metabolism and cerebral blood volume (CBV), decreases ICP, and increases CPP. Evidence of the impact of moderate hypothermia on the outcome of patients with TBI was controversial. Initially, studies showed that moderate hypothermia, established on admission, was associated with significantly improved outcome at 3 and 6 months after TBI. However, in a large RCT, no effect of moderate hypothermia has been demonstrated on outcome after TBI.

The National Acute Brain Injury Study: Hypothermia II was a randomized, multicenter clinical trial of patients with severe TBI who were enrolled within 2 to 5 hours of injury. Patients were randomly assigned to hypothermia (cooling to 33°C for 48 hours) or normothermia. There was no significant difference in outcomes between the hypothermia and the normothermia groups. The trial did not confirm the utility of

34 nursece4less.com nursece4less.com nursece4less.com nursece4less.com hypothermia as a primary neuroprotective strategy in severe TBI patients. However, temperature should be controlled and fever should be aggressively treated in patients with severe TBI. Moderate hypothermia may be used in refractory, uncontrolled ICP.

Mechanical Patients with severe TBI are usually intubated and Ventilation mechanically ventilated. Hypoxia, defined as O2saturation < 90%, or PaO2 < 60 mmHg, should be avoided. Prophylactic hyperventilation to a PaCO2 < 25 mmHg is not recommended. Within the first 24 hours following severe TBI, hyperventilation should be avoided, as it can further compromise an already critically reduced cerebral perfusion.

Coles, et al., reported that, in patients with TBI, hyperventilation increases the volume of severely hypoperfused tissue within the injured brain, despite improvements in CPP and ICP. These reductions in regional cerebral perfusion may represent regions of potentially ischemic brain tissue.

Excessive and prolonged hyperventilation results in cerebral vasoconstriction and ischemia. Thus, hyperventilation is recommended only as a temporizing measure to reduce an elevated ICP. A brief period (15-

30 minutes) of hyperventilation, to a PaCO2 30-35 mm Hg is recommended to treat acute neurological deterioration reflecting increased ICP.

Longer periods of hyperventilation might be required for intracranial hypertension refractory to all treatments including sedation, paralytics, CSF drainage, hypertonic saline solutions (HSSs) and osmotic diuretics. However, when hyperventilation is used,

SjvO2 or PbtO2 measurements are recommended to monitor cerebral oxygenation and avoid cerebral ischemia. The ventilatory settings should be adjusted to maintain a pulse oximetry (SpO2) of 95% or greater and/or PaO2 of 80 mmHg or greater and to achieve normoventilation (eucapnia) with PaCO2 of 35 to 40 mmHg.

Mascia, et al., reported that high tidal volume ventilation is an independent predictor and associated with acute lung injury (ALI) in patients with severe TBI. Hence, protective ventilation with low tidal volume and moderate positive end-expiratory pressure (PEEP) has been recommended to prevent ventilator- associated lung injury and increased ICP. Prior to suctioning the patient through the endotracheal tube (ETT), preoxygenation with a fraction of inspired oxygen (FiO2) = 1.0, and

35 nursece4less.com nursece4less.com nursece4less.com nursece4less.com administration of additional sedation are recommended to avoid desaturation and sudden increase in the ICP.

Suctioning ETT must be brief and atraumatic. It has been suggested that PEEP increases intrathoracic pressure leading to a decrease in cerebral venous drainage and consequently to an increase in CBV and ICP. However, the effect of PEEP on ICP is significant only with level of PEEP higher than 15 cm H2O in hypovolemic patients. Nevertheless, the lowest level of PEEP, usually 5 to 8 cm H2O that maintains adequate oxygenation and prevents end-expiratory collapse, should be used.

Higher PEEP, up to 15 cm H2O, may be used in cases of refractory hypoxemia. A significant number of patients with severe TBI develop ALI or acute respiratory distress syndrome (ARDS), with an incidence of ALI/ARDS reported between 10% and 30%. Etiology of ALI/ARDS in patients with severe TBI include aspiration, pneumonia, , massive blood transfusion, transfusion-related ALI (TRALI), sepsis, neurogenic and use of high tidal volume and high respiratory rate.

Development of ALI/ARDS in patients with severe TBI is associated with longer ICU LOS and fewer ventilation free days. Ventilatory management of patients with severe TBI and ALI/ARDS is challenging.

A balanced ventilation strategy, between the guidelines for severe TBI or the historical "brain injury" approach (adequate oxygenation: optimizing oxygenation- preserving cerebral venous drainage by using low levels of PEEP, and mild hypocapnia by using high tidal volume), and the lung protective ventilation strategy (by using high PEEP and low tidal volume), is desired, however, is difficult to achieve.

Permissive hypercapnia, an acceptable strategy in patients with ALI/ARDS, should be avoided, if possible, in patients with severe TBI because of the associated cerebral vasodilatation, increased CBV and ICP.

Venous TBI patients are at increased risk for venous Thromboembolism thromboembolism (VTE). In some cases, antiembolic Prophylaxis stockings or pneumatic compression devices may be used. Once the risk of hemorrhage passes, low molecular- weight heparin may be given. Also, inferior venal caval filters may be placed transvenously. Screening duplex ultrasound studies of the legs may be done to help identify VTE. If VTE occurs, carry out appropriate interventions. Mechanical

36 nursece4less.com nursece4less.com nursece4less.com nursece4less.com thromboprophylaxis, including graduated compression stockings and sequential compression devices, are recommended unless their use is prevented by lower extremity injuries. The use of such devices should be continued until patients are ambulatory.

In the absence of a contraindication, low molecular weight heparin (LMWH) or low dose unfractionated heparin should be used in combination with mechanical prophylaxis. However, the use of pharmacological prophylaxis is associated with an increased risk for expansion of . Although, evidence to support recommendations regarding the timing of pharmacological prophylaxis is lacking, most experts suggest initiating pharmacologic prophylaxis as early as 48 to 72 hours after the injury, in the absence of other contraindications.

Seizure Prophylaxis TBI may increase the risk of non-epileptic seizures in a small number of patients. Seizures that immediately follow the injury or arise during the early post-injury phase presumably are a reaction to the initial trauma; those arising more than 2 weeks after injury are thought to stem from permanent changes in brain structure. Although the seizure risk is low, seizures increase metabolic activity and oxygen demands, which may further compromise the damaged brain.

Routine seizure prophylaxis later than 1 week after a TBI isn’t recommended. However, if needed, phenytoin or valproate can be given. Post-traumatic seizures are classified as early occurring within 7 days of injury, or late occurring after 7 days following injury. Prophylactic therapy (phenytoin, carbamazepine, or phenobarbital) is not recommended for preventing late post-traumatic seizures. However, the BTF recommended prophylaxis therapy to prevent early post-traumatic seizure in TBI patients who are at high risk for seizures.

The risk factors include: GCS score < 10, cortical contusion, depressed skull fracture, subdural hematoma, , intracerebral hematoma, penetrating TBI, and seizures within 24 hours of injury. Phenytoin is the recommended drug for the prophylaxis of early post-traumatic seizures. A loading dose of 15 to 20 mg/kg administered intravenously over 30 minutes followed by 100 mg, IV, every 8 hours, titrated to plasma level, for 7 days, is recommended. Patients receiving antiseizures prophylaxis should be monitored for potential side effects.

37 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Hemodynamic Hemodynamic instability is common in patients with Support severe TBI. Hypotension, defined as SBP < 90 mm Hg or MAP < 65 mmHg, is a frequent and detrimental secondary systemic brain insult and has been reported to occur in up to 73% during ICU stay. Studies from the Traumatic Coma Data Bank (TCDB) documented that hypotension is a major determinant and an independent predictor of outcome of severe TBI.

Hypotension is significantly associated with increased mortality following TBI. Among predictors of outcome of TBI, hypotension is the most amenable to prevention, and should be scrupulously avoided and aggressively managed.

It is unlikely that an isolated TBI by itself would cause hypotension unless the patient has become brain dead. Intravascular volume depletion due to hemorrhage from associated injuries such as scalp, neck, vessels, chest, abdomen, pelvis and extremities, or due to polyuria secondary to diabetes insipidus, are the most common causes of hypotension in patients with severe TBI. Other potential reasons for hypotension in patients with severe TBI are myocardial contusion resulting in primary pump failure, and spinal cord injury with spinal shock (cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrythmias). An often missed cause of hypotension in patients with TBI is the use of etomidate for intubation. It has been reported that even a single dose of etomidate may cause adrenal insufficiency resulting in hypotension.

Appropriately aggressive fluid administration to achieve adequate intravascular volume is the first step in resuscitating a patient with hypotension following severe TBI. The CVP may be used to guide fluid management and is recommended to be maintained at 8 - 10 mmHg. In patients who respond poorly to adequate volume expansion and vasopressors, demonstrate hemodynamic instability, or have underlying cardiovascular disease, a pulmonary artery catheter or non-invasive hemodynamic monitoring may be considered. The pulmonary capillary wedge pressure should be maintained at 12 - 15 mmHg. Several reliable predictors of fluid responsiveness such as pulse pressure variation, systolic pressure variation, stroke volume variation, and collapse of inferior vena cava have been suggested to guide fluid management. Isotonic crystalloids, specifically normal saline (NS) solution are the fluid of choice for fluid resuscitation and volume replacement. HSSs are effective for blood pressure restoration in hemorrhagic shock; however,

38 nursece4less.com nursece4less.com nursece4less.com nursece4less.com with no survival benefit. The National Heart, Lung, and Blood Institute of the National Institutes of Health has stopped enrollment into a clinical trial testing the effects of HSSs on patients with severe TBI because HSS was no better than the standard treatment of NS. Blood and blood products may be used as appropriate.

Hyperosmolar Mannitol administration is an effective method to Therapy decrease raised ICP after severe TBI. Mannitol creates a temporary osmotic gradient and it increases the

serum osmolarity to 310 to 320 mOsm/kg H2O. The prophylactic administration of mannitol is not recommended.

Prior to ICP monitoring, mannitol use should be restricted to patients with signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial causes. Arbitrarily, mannitol should not be administered if serum osmolarity is > 320 mOsm/kg H2O. Osmotic diuresis should be compensated by adequate fluid replacement with isotonic saline solution to maintain euvolmia. The effective dose is 0.25-1 g/kg, administered intravenously over a period of 15 to 20 minutes.

The regular administration of mannitol may lead to intravascular dehydration, hypotension, pre-renal azotemia and hyperkalemia. Mannitol may pass and accumulate in the brain, causing a reverse osmotic shift or rebound effect, and raising brain osmolarity, thus increasing ICP. Mannitol is contraindicated in patients with TBI and renal failure because of the risk of pulmonary edema and heart failure.

HSSs have been suggested as alternative to mannitol. HSS has a number of beneficial effects in head-injured patients, including expansion of intravascular volume, extraction of water from the intracellular space, decrease in ICP, and increase in cardiac contractility. HSS produces osmotic dehydration and viscosity- related cerebral vasoconstriction. Prolonged administration of a HSS was associated with lowered ICP, controlled cerebral edema, with no adverse effects of supraphysiologic hyperosmolarity such as renal failure, pulmonary edema, or central pontine demyelination. In a recent meta-analysis, Kamel, et al., found that hypertonic saline is more effective than, and may be superior to the current standard of care which is, mannitol for the treatment of elevated ICP. Steroids Steroids administration is not recommended for improving the outcome or reducing ICP in patients with severe TBI. Moreover, steroids may be harmful after TBI. The CRASH trial, a multicenter international

39 nursece4less.com nursece4less.com nursece4less.com nursece4less.com collaboration, aimed to confirm or refute such an effect by recruiting 20,000 patients. In May, 2004, the data monitoring committee disclosed the unmasked results to the steering committee, which stopped recruitment at 10,008 patients.

Compared with placebo, the risk of death from all causes within 2 weeks was higher in the group allocated (21.1% vs. 17.9% deaths; relative risk = 1.18. No reduction in mortality with methylprednisolone in the 2 weeks after head injury was found. The cause of the rise in risk of death within 2 weeks was unclear. Hence, in patients with severe TBI, high-dose methylprednisolone is contraindicated.

Nutrition Severe TBI patients are usually in hypermetabolic, hypercatabolic and hyperglycemic state, with altered G.I. functions. There is evidence suggesting that malnutrition increases mortality rate in TBI patients. Studies documented the superiority of enteral feeding over parenteral nutrition (PN).

Use of PN should be limited to contraindications of enteral feeding, as it is associated with complications and an increased mortality. Hence, early enteral feeding is recommended in patients with severe TBI, as it is safe, cheap, cost-effective, and physiologic. The potential advantages of enteral feeding include stimulation of all gastro-intestinal tract functions, preservation of the immunological gut barrier function and intestinal mucosal integrity, and reduction of and septic complications.

Frequently, patients with severe TBI have gastric feeding intolerance due to many reasons including abnormal gastric emptying and altered gastric function secondary to increased ICP, and use of opiates. Prokinetic agents such as metoclopramide or erythromycin, improve tolerance. Post-pyloric feeding avoids gastric intolerance and allows higher caloric and nitrogen intake. There is growing body of evidence suggesting the benefit of a lower caloric intake.

Initially, a nasogastric or orogastric tube is inserted to decompress the stomach and reduce the aspiration risk. (Typically, the nasal route is avoided as it can obstruct sinus drainage, leading to sinusitis or VAP.)

TBI patients have increased metabolic demands, so parenteral or enteral nutrition should begin as soon as tolerated. Nutritional target goals should be met by day 7. A small-bore feeding tube may be placed into the small intestine or a percutaneous gastrostomy tube

40 nursece4less.com nursece4less.com nursece4less.com nursece4less.com may be used to deliver nutrition and decrease the aspiration risk.

Glycemic Control In patients with severe TBI, stress hyperglycemia is a common secondary systemic brain insult. Studies showed that hyperglycemia has repeatedly been associated with poor neurological outcome after TBI. Although hyperglycemia is detrimental, maintaining low blood glucose levels within tight limits is controversial in patients with severe TBI, because hypoglycemia, a common complication of tight glucose control, can induce and aggravate underlying brain injury. Vespa, et al., reported that intensive insulin therapy (IIT) results in a net reduction in microdialysis glucose and an increase in microdialysis glutamate and lactate/pyruvate ratio without conveying a functional outcome advantage. Oddo, et al., documented that tight systemic glucose control is associated with reduced cerebral extracellular glucose availability and increased prevalence of brain energy crisis, which in turn correlates with increased mortality. IIT may impair cerebral glucose metabolism after severe brain injury.

A recent meta-analysis on IIT in brain injury revealed that IIT did not appear to decrease the risk of in- hospital or late mortality. Moreover, IIT did not have a protective effect on long-term neurological outcomes. However, IIT increased the rate of hypoglycemic episodes. Consequently, the majority of currently available clinical evidence does not support tight glucose control (maintenance of blood glucose levels below 110-120 mg/dl) during the acute care of patients with severe TBI.

Positioning In patients with increased ICP, frequent turning and repositioning may not be possible. As ordered, keep the head of the bed elevated at least 30 degrees with the patient’s neck in neutral alignment, to promote venous drainage of the brain and reduce brain swelling. This position also decreases the risk of aspiration and VAP. A patient with impaired oxygenation and ventilation may be placed on a kinetic therapy bed or may be positioned prone. During patient turning and repositioning, take measures to prevent skin breakdown.

Summary

41 nursece4less.com nursece4less.com nursece4less.com nursece4less.com In some cases, a patient with head trauma will present with critical injuries that require specialized interventions and care. The range of actions include stabilization through treatment for a specific injury, which may require surgery. Assessment and treatment of traumatic brain injury should begin as soon as possible. Therefore, emergency personnel are often the first individuals who assess and treat the injury. Typically, treatment begins as soon as emergency responders arrive on the scene or as soon as an individual arrives at the emergency room. The key components of the trauma assessment include the airway assessment, skull examination, patient history, and neurological examination.

The management of severe traumatic brain injury centers on meticulous and comprehensive intensive care that includes a multi-model, protocolized approach involving careful hemodynamic support, respiratory care, fluid management, and other aspects of therapy, aimed at preventing secondary brain insults, maintaining an adequate cerebral perfusion pressure, and optimizing cerebral oxygenation. This approach clearly requires the efforts of a multidisciplinary team. While such management can be challenging, it is by all means rewarding considering the potentially devastating impact of the problem.

Please take time to help NurseCe4Less.com course planners evaluate the nursing knowledge needs met by completing the self-assessment of Knowledge Questions after reading the article, and providing feedback in the online course evaluation.

Completing the study questions is optional and is NOT a course requirement. 1. When swelling and fluid accumulation occur within the brain, it can be extremely dangerous for the patient primarily because this accumulation

42 nursece4less.com nursece4less.com nursece4less.com nursece4less.com

a. creates lesions within the brain. b. creates pressure in the brain. c. blocks the brain-blood barrier. d. may lead to infection.

2. True or False: Once intracranial pressure (ICP) becomes elevated, the only option for treatment is a ventriculostomy.

a. True b. False

3. Patients with low risk head injuries may display symptoms such as

a. persistent emesis. b. severe headache. c. anterograde amnesia. d. None of the above

4. When a patient is released to a caregiver for monitoring the injury at home, the home caregiver should

a. check the patient once a day. b. assess the patient every two hours. c. assess the patient each morning. d. take the patient for outpatient assessment.

5. Cranial nerve and pupillary examination includes assessing a patient’s

a. level of consciousness. b. posture. c. gag reflex. d. pain sensations.

6. Head trauma due to ______is more complex than other forms of head trauma.

a. rotational force

43 nursece4less.com nursece4less.com nursece4less.com nursece4less.com b. skull fractures c. blast trauma d. an open injury

7. Initial assessment of a patient with a head trauma injury includes

a. measuring a patient’s level of consciousness. b. checking the extent of skull fractures. c. using the Glasgow Coma Scale. d. measuring reflexes.

8. Using the Glasgow Coma Scale, a patient’s score of ______points is classified as severe brain injury.

a. 3 to 8 b. 13 to 15 c. 9 to 12 d. 15 or more

9. Which of the following diagnostic tools is not used during an emergency assessment of a patient’s traumatic brain injury?

a. An X-ray b. Diffusion tensor imaging c. A CT scan d. An MRI

10. True or False: Regardless of the type of injury (blunt or penetrating, open or closed) the initial examination will be conducted as soon as possible and will often occur in conjunction with resuscitation.

a. True b. False

11. Hemotympanum or bruising over the mastoid, known as Battle’s sign, suggests

a. a basal skull fracture. b. cranial nerve palsy.

44 nursece4less.com nursece4less.com nursece4less.com nursece4less.com c. a middle fossa fracture. d. anterior fossa fracture.

12. It is not usually recommended to test ______in a head-injured patient owing to the high risk of associated cervical spinal injury.

a. oculocephalic reflexes b. cranial nerve palsy c. pupillary reactions d. accommodation reflex

13. True or False: Using descriptive words (e.g., semi-conscious or coma) to describe and assess a patient’s state of consciousness is superior to the Glasgow Coma Scale (GCS) because descriptive words are more precise.

a. True b. False

14. Which cranial nerve is the most commonly affected cranial nerve after head injury?

a. Optic nerve b. Trochlear nerve c. Abducens nerve d. Olfactory nerve

15. The loss of the sense of taste after a head injury is

a. tested by stimulating the supraorbital nerve. b. due to damage to the abducens nerve. c. usually due to anosmia. d. tested regularly to assess damage to the trochlear nerve.

16. Intracranial pressure can be subatmospheric

a. in newborns. b. in young children. c. under the Monroe-Kellie hypothesis.

45 nursece4less.com nursece4less.com nursece4less.com nursece4less.com d. when a temporal mass lesion is present.

17. ______is the preferred device for monitoring intracranial pressure (ICP) and the standard against which all newer monitors are compared.

a. The MRI b. The X-ray c. The CT scan d. The ventriculostomy catheter

18. One of the disadvantages of a ventriculostomy is

a. it has no therapeutic value. b. its high cost. c. difficulties inserting catheter into displaced ventricles. d. its ability to recalibrate.

19. Patients with traumatic brain injury are particularly at risk for developing elevated intracranial pressure if their Glasgow Coma Scale score is ______after cardiopulmonary resuscitation and who have an abnormal admission head CT scan.

a. 8 or less b. 15 or higher c. 10 to 12 d. 9 or above

20. The jugular venous oxygen saturation (SjvO2) is an indicator of

a. intracranial pressure (ICP). b. cerebral oxygenation and cerebral metabolism. c. compressed or displaced ventricles. d. a loss of cerebrospinal fluid.

CORRECT ANSWERS:

1. When swelling and fluid accumulation occur within the brain, it can be extremely dangerous for the patient primarily because this accumulation

46 nursece4less.com nursece4less.com nursece4less.com nursece4less.com

b. creates pressure in the brain.

“... when swelling and fluid accumulation occur within the brain, it can be extremely dangerous for the patient. The danger arises because the skull limits the space for the brain to expand so that swelling and fluid accumulation elevates intracranial pressure (ICP).”

2. True or False: Once intracranial pressure (ICP) becomes elevated, the only option for treatment is a ventriculostomy.

b. False

“This information is closely monitored so that action can be taken if the ICP reaches an alarming level. If this occurs, the patient may have to undergo a ventriculostomy. This procedure is used to drain cerebrospinal fluid as a way to reduce pressure on the brain. In some instances, pharmacological agents may be used to decrease ICP. These drugs include mannitol and barbiturates.”

3. Patients with low risk head injuries may display symptoms such as

a. persistent emesis. b. severe headache. c. anterograde amnesia. d. None of the above [correct answer]

“Patients who display symptoms of low risk injuries will not require extensive treatment.... Moderate risk injuries typically include the following symptoms of persistent emesis, severe headache, anterograde amnesia, loss of consciousness, and signs of intoxication.”

4. When a patient is released to a caregiver for monitoring the injury at home, the home caregiver should

b. assess the patient every two hours.

47 nursece4less.com nursece4less.com nursece4less.com nursece4less.com “When a patient is released, thorough instructions should be given to the patient and caregivers for monitoring the injury at home. The home caregiver should wake the patient every two hours to provide a thorough assessment.”

5. Cranial nerve and pupillary examination includes assessing a patient’s

c. gag reflex.

“Cranial Nerve and Pupillary Examination: This reflects brainstem function. Assess the pupils, eye movements, cough reflex, corneal reflex and gag reflex.”

6. Head trauma due to ______is more complex than other forms of head trauma.

c. blast trauma

“For example, blast trauma related head trauma is more complex than other forms of head trauma. Due to the complexity of blast related head injury, the assessment and treatment can be difficult to administer and determine.”

7. Initial assessment of a patient with a head trauma injury includes

d. measuring reflexes.

“Primary assessment includes measuring vital signs and reflexes, as well as administering a thorough neurological exam. The initial exam includes checking the patient’s temperature, blood pressure, pulse, breathing rate, pupil size and response to light.”

8. Using the Glasgow Coma Scale, a patient’s score of ______points is classified as severe brain injury.

a. 3 to 8

48 nursece4less.com nursece4less.com nursece4less.com nursece4less.com “This assessment is done using the Glasgow Coma Scale, which is a standardized, 15-point test that measures neurologic functioning using three assessments: eye opening, best verbal response, and best motor response. These measures are used to determine the severity of the brain injury. A score of 13 to 15 is classified as mild, 9 to 12 as moderate, and 3 to 8 as severe.”

9. Which of the following diagnostic tools is not used during an emergency assessment of a patient’s traumatic brain injury?

d. An MRI

“MRI’s are not used during the initial emergency assessment as they require a significant amount of time and are not always available during the initial assessment. However, an MRI is an important diagnostic tool and should be used when appropriate and available.”

10. True or False: Regardless of the type of injury (blunt or penetrating, open or closed) the initial examination will be conducted as soon as possible and will often occur in conjunction with resuscitation.

a. True

“Regardless of the type of injury (blunt or penetrating, open or closed) the initial examination will be conducted as soon as possible and will often occur in conjunction with resuscitation.”

11. Hemotympanum or bruising over the mastoid, known as Battle’s sign, suggests

c. a middle fossa fracture.

“Hemotympanum or bruising over the mastoid (Battle’s sign) suggests a middle fossa fracture.”

12. It is not usually recommended to test ______in a head-injured patient owing to the high risk of associated cervical spinal injury.

a. oculocephalic reflexes

49 nursece4less.com nursece4less.com nursece4less.com nursece4less.com “It is not usually recommended to test oculocephalic reflexes in a head-injured patient owing to the high risk of associated cervical spinal injury.”

13. True or False: Using descriptive words (e.g., semi-conscious or coma) to describe and assess a patient’s state of consciousness is superior to the Glasgow Coma Scale (GCS) because descriptive words are more precise.

b. False

“Using purely descriptive methods to assess conscious state is problematic. One observer’s ‘somnolent’ is another’s ‘drowsy.’ When is a person stuporous and when are they obtunded? What is semi-conscious and when does a clouded conscious state become coma? Consciousness is a continuum and clinicians use the Glasgow Coma Scale (GCS) as a measure (albeit crude) of level of consciousness.”

14. Which cranial nerve is the most commonly affected cranial nerve after head injury?

d. Olfactory nerve

“Many of the cranial nerves can be assessed even in the unconscious patient. I (olfactory): Assessment obviously requires cooperation, but this nerve should be examined when possible, as it is the most commonly affected cranial nerve after head injury and is often ignored.”

15. The loss of the sense of taste after a head injury is

c. usually due to anosmia.

“Taste is not usually tested. Patients often complain of loss of taste after a head injury but this is usually due to anosmia.”

16. Intracranial pressure can be subatmospheric

a. in newborns.

“Intracranial pressure can be subatmospheric in newborns.”

50 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 17. ______is the preferred device for monitoring intracranial pressure (ICP) and the standard against which all newer monitors are compared.

d. The ventriculostomy catheter

“The ventriculostomy catheter is the preferred device for monitoring ICP and the standard against which all newer monitors are compared.”

18. One of the disadvantages of a ventriculostomy is

c. difficulties inserting catheter into displaced ventricles.

“An intraventricular catheter is connected to an external pressure transducer via fluid-filled tubing. The advantages of the ventriculostomy are its relatively low cost, the option to use it for therapeutic CSF drainage, and its ability to recalibrate to minimize errors owing to measurement drift. The disadvantages are difficulties with insertion into compressed or displaced ventricles, inaccuracies of the pressure measurements because of obstruction of the fluid column, and the need to maintain the transducer at a fixed reference point relative to the patient’s head.”

19. Patients with traumatic brain injury are particularly at risk for developing elevated intracranial pressure if their Glasgow Coma Scale score is ______after cardiopulmonary resuscitation and who have an abnormal admission head CT scan.

a. 8 or less

“Monitoring of ICP is an invasive technique and has some associated risks. For a favorable risk-to-benefit ratio, ICP monitoring is indicated only in patients with significant risk of intracranial hypertension. Patients with TBI who are particularly at risk for developing an elevated ICP include those with Glasgow Coma Scale of 8 or less after cardiopulmonary resuscitation and who have an abnormal admission head CT scan.” 20. The jugular venous oxygen saturation (SjvO2) is an indicator of

b. cerebral oxygenation and cerebral metabolism.

“The jugular venous oxygen saturation (SjvO2) is an indicator of both cerebral oxygenation and cerebral metabolism, reflecting the

51 nursece4less.com nursece4less.com nursece4less.com nursece4less.com ratio between cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2).”

Reference Section

The References below include published works and in-text citations of published works that are intended as helpful material for your further reading. [These References are for a multi-part series on Neuroscience Critical Care.]

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