Session Number 311

CCRN-PCCN-CMC REVIEW: NEURO PART 1

Cynthia Blank-Reid, RN, MSN, CEN, CNRN

Trauma Clinical Nurse Specialist
Temple University Hospital
Philadelphia, PA

Content Description

This course prepares the critical care nurse for successful completion of the CCRN and PCCN
examinations. In accordance with the AACN test plans for the CCRN and PCCN, this
lecture will discuss the neurological illnesses and injuries identified on the blue print with an
emphasis on possible questions that may be asked on these subjects in the examination. This
lecture will discuss neurologic assessment, presentation and treatment of increased intracranial
pressure,, head injury, and neurologic infections. There will be time allotted for sample
questions to be discussed during the lecture.

Learning Objectives
At the end of this session, the participant will be able to:

1. Describe the primary treatment modalities used to treat control intracranial hypertension.
2. Discuss identification and treatment of traumatic brain injuries
3. Describe presentation and treatment of neurologic infections

REFERENCES
NOTE: Please refer to outline for references pertaining to this session
 CCRN-PCCN-CMC REVIEW: NEURO PART 1
Cynthia Blank-Reid, RN, MSN, CEN, CNRN
Trauma Clinical Nurse Specialist
Temple University Hospital
Philadelphia, PA

CCRN and PCCN CCRN only

Intracranial hemorrhage (subarachnoid, Aneurysm, AV malformation
epidural, subdural Encephalopathy
Seizure disorders Head trauma
Stroke Neurologic infections
ICP monitoring
Neurosurgery

Note for PCCN candidates: This presentation includes discussions of advanced devices such as
ICP monitoring and administration of vasoactive medications. These topics will not be tested in
the PCCN exam

Exam Tip: Approximately 12% of the CCRN exam and 5% of the PCCN exam will focus on the
neurologic system, which is 18 and 6 questions respectively.

I. Care of the patient with increased intracranial pressure (IICP)

A. Monroe-Kellie Hypothesis
1. Skull (non-compliant box)
2. 3 components
Brain (80% of skull)
Blood (10% of skull)
CSF (10% of skull)
3. Hypothesis
If there is an increase in the volume of one of the components, it must be
offset by an equal decrease of one or both of the other components in
order for the ICP to remain normal
If an increase in the volume of one of the components is not offset by an
equal decrease in one or both of the other components, the ICP will
increase
B. Causes of Increased ICP
1. Increased brain volume
2. Increased blood volume
3. Increased CSF volume
4. Space occupying lesions
C. ICP Regulation: Compensation and Autoregulation
1. Compensation
Variety of initial responses that occur in an attempt to keep pressure in the
normal range when there are small increases in ICP
Finite
Affected by both the size of the mass and the rate of expansion
 Shunt CSF into the subarachnoid (SA) space
Increase CSF absorption in the venous sinus
Decrease of CSF production
Decrease of blood volume by altering cerebral blood flow (CBF)
Skull expansion (infants only)
2. Cerebral Autoregulation
Maintains adequate cerebral blood flow by constriction or dilatation of
cerebral arteries in response to changes in
Systemic blood flow (blood pressure)
Carbon dioxide (C02)
Systemic Blood Flow
Increased
Cerebral arteries constrict
Fails with MAP>160
Decreased
Cerebral arteries dilate
Fails with MAP<60
Carbon Dioxide
Arterial C02 content has an extremely potent effect on CBF by
causing changes in the cerebral pH, leading to changes in the
resistance of cerebral vessels
Potent cerebral vasodilator
Increased
Cerebral arteries dilate
Increase in volume can increase ICP
Decreased
Cerebral arteries constrict
Decrease in volume can decrease ICP
Cerebral ischemia
D. Decompensation
1. Failure of compensation and autoregulation to keep ICP WNL may lead to:
Decrease in CBF
Decrease in CPP
Cerebral ischemia/edema
Brain death
2. Compliance
Ability of the brain to accommodate changes in intracranial volume, without
significant changes in ICP
Normal compliance
Small increases in intracranial volume result in no or little increase in
ICP
Decreased compliance
Small increases in intracranial volume
result in large increases in ICP
3. Pressure Volume Curve
When compliance has reached its limit, a state
 of decompensation with increased ICP results. As the ICP rises, the
relationship between volume and pressure changes, and small increases in
volume may cause major elevations in ICP.
5. Clinical Scenarios Causing IICP
Space occupying lesions
Subdural, epidural, intracerebral hematomas
Abscesses
Tumors
Hemorrhagic Stroke
Cytotoxic edema
Intracellular swelling
Cellular hypoxia
Hydrocephalus
Acute hypo-osmolality
Water intoxication (SIADH)
Vasogenic cerebral edema
Direct injury
Hypoxic injury
Severe hypertension
Inflammatory mediators
May see with contusions, tumors, abscesses, meningitis, diffuse brain
injury
Ischemic Stroke
E. Signs and Symptoms of IICP
1. Early Signs and Symptoms of IICP
LOC change: restless, agitated, confused
Headache
Nausea and projectile vomiting
Visual changes: blurred vision, diplopia
Pupillary changes: sluggish pupils, ipsilateral changes
2. Late Signs and Symptoms of IICP
LOC Deterioration: difficult to arouse, coma
Pupillary changes: fixed, dilated
Alteration in temperature
Respiratory irregularities
Impaired brainstem reflexes
Cushings triad:
Bradycardia
Systolic hypertension
Widened pulse pressure
Posturing
3. Assessment of Increased ICP
F. Level of Consciousness = Awareness of self and environment
a. General behavior
b. Appearance
c. Appropriateness to the situation
 d. Attention span
e. Long and short term memory, insight, orientation and calculation
f. Emotional state, affect
g. Though content: illusions, hallucinations, delusions
h. Execution of intentional motor activity
Inability = apraxia
i. Recognition and interpretation of sensations
j. Language
Fluency, clarity, content, comprehension of written and
spoken word
Ability to name objects and repeat phrases
Patient awareness of language disorder
Receptive aphasia (Wernickes aphasia) Comprehension
of speech impaired. Able to make words, but will
be nonsensical, rambling. Unable to identify
written words.
Expressive aphasia (Brocas aphasia) Deficit in language
output or speech production
May be mild if due to weakness or lack of
coordination of muscles of speech (dysarthria)
Incorrect intonation or phrasing
Most severe inability to communicate thorough
verbal and written means or gesturing
2. Muscle strength
a. Able to follow commands
Grade strength on 0 to 5 scale
O = Absent, no muscle contraction
1 = Contraction of muscles felt or seen
2 = Movement through full rang of motion with gravity
removed
3 = Movement through full range of motion against gravity
4 = Movement against resistance but can be overcome
5 = Full strength against resistance
b. Unable to follow commands
Observe which extremities move spontaneously or to noxious
stimuli
Hemiparesis or hemiplegia may be detect by lifting both
arms off bed and releasing simultaneously
Limb on hemiparetic side will fall more quickly and
more limply
c. Pathologic movements
Primitive
Grasp in response to stimulation of palm
Sucking In response to lip stimulation
Rooting Mouth opens, head deviates toward a stimulus
applied to the lower lip or cheek
 Babinski
Stroking the lateral aspect of the sole of foot from heel up
and across ball of foot causes abnormal dorsiflexion of the great
toe and extensor fanning of the other toes.
3. Pupil abnormalities
a. Indicates area of brain affected
b. Small, equal, reactive
c. Nonreactive, midpositional
d. Fixed and dilated
e. Bilateral fixed and dilates
f. Pinpoint, nonreactive
g. One pupil small than other, both reactive
4. Vital signs
a. Temperature neurogenic fever can be caused by damage to
hypothalamus
b. Respiratory patterns - Indicate area of brain affected
Cheyne-Stokes regular cycles of respiration that gradually
increase in depth to and then decrease to periods of apnea
Central neurogenic hyperventilation Deep, rapid respirations
Apneustic Prolonged inspiration followed by 2 to 3 second pause
Cluster of irregular breaths followed by apneic period lasting a
variable amount of time
Ataxic Irregular, unpredictable pattern of shallow and deep
respirations and pauses
c. Pulse and blood pressure
Unreliable in detecting CNS disease or neurologic deterioration
Changes usually late indication of increased ICP
Cushings response
Compensatory response that attempts to provide adequate
CPP in the presence of rising ICP
Bradycardia, systolic hypertension, bradypnea
Late and poor prognostic sign
5. Glasgow Coma Scale Total score ranges 3-15
Eye Opening Assesses arousal state
4 Spontaneously Patient opens eyes without stimulation
3 To voice Patient opens eyes when spoken to
2 To pain Patient opens eyes when a noxious stimulus is
applied
1 None Patient does not open eyes to any stimulus
Best Verbal Assesses the content of consciousness in terms
Response of the ability to produce speech and quality of
speech
5 Oriented Patient can state his or her name, where he or she
is, and the date
4 Confused Patient speaks words but cannot state either who
he or she is, where he or she is, or the date
 3 Inappropriate Patient speaks words with no specific intent at
words communicating
2 Incomprehensi Patient grunts, groans, or makes other sounds
ble sounds
1 None Patient makes no attempt to vocalize (a T may
be written after the score to indicate the presence
of a tracheal tube)
Best Motor Assesses both arousal and the content of
Response consciousness.
6 Obeys Follows commands
5 Localizes Attempts to remove noxious stimulus
4 Withdraws Pulls away from noxious stimulus
3 Abnormal Decorticate posturing
flexion
2 Abnormal Decerebrate posturing
extension
1 No response No motor movement of any kind to any stimulus

Decorticate posturing Decerebrate posturing

G. Herniation Syndromes
1. Shifting of brain tissue from one compartment to another, caused by increased
ICP and a loss of autoregulation and compensation mechanisms
2. Protrusion of a portion of the brain through an abnormal opening
3. Types of Brain Herniations:
- Occurs with high ICP; death follows without rapid intervention
Supratentorial
Cingulate/Subfalcine (1)
- Shift of brain tissue of one cerebral
hemisphere under the falx cerebri to the other
cerebral hemisphere
Uncal/Lateral Transtentorial (2)
- Lesion above tentorium forces uncus
of temporal lobe to displace through the
tentorial notch.
Central Transtentorial (3)
- Downward shift of cerebral hemispheres, basal ganglia, and
diencephalon through the tentorial notch
 Infratentorial
Tonsillar herniation (4)
- Cerebellar tonsils displaced through the foramen magnum
H. Increased ICP
1. Normal ICP = 0-15mmHg
2. Moderately Increased ICP = 15-40 mmHg
3. Severely Increased ICP 40 mmHg
4. ICP treatment should be initiated at an upper threshold of 20 - 25 mmHg
5. Cerebral Perfusion Pressure (CPP)
The pressure required to perfuse brain
CPP = MAP - ICP
Normal range: 60-100 mmHg
Decreased: Less than 60 mmHg
Autoregulation fails
Cerebral ischemia
With IICP, goal is CPP >70 mmHg
6. ICP Monitoring:
Anatomic Locations
Epidural
Subdural
Subarachnoid
Intraparenchymal
Intraventricular
7. ICP Monitoring Systems
Fluid filled catheter (external transducer system)
Fiberoptic transducer
Ventriculostomy Drainage System
Document character, amount, and turbidity of drainage
Monitor system for air bubbles
Drain CSF as indicated for IICP
Maintain sterility of system
8. ICP Waveforms
Originates as pulsations in the choroidal plexuses of the ventricles
Corresponds with each heartbeat
ICP Waveforms
A or Plateau waves
B waves
C waves
Components of the ICP Waveform
P1 - Percussion wave
P2 - Tidal wave
P3 - Dicrotic wave
I. Nursing Management of Increased ICP
1. Based on institutional policies:
Dressing change
External drainage system
 CSF sampling
2. Sterile technique when opening an ICP monitoring system
3. Vigilant neurological assessments
Usually every hour
Complete neuro assessments are the key to catching changes in the
patients condition
At change of shift, both nurses do the assessment together
Assures continuity of care
Validation of findings from shift to shift
4. Maintain patent airway and adequate ventilation
Suction after adequate pre-oxygenation and hyperventilation
5. Position the patient to promote venous return
Head midline
HOB 30 degrees
No ETT tape behind the head
6. Minimize clustering of nursing care and do only what is necessary at that time
7. Maintain a quiet and dim environment to decrease stimulation
8. Provide emotional support to both patient and family
J. Medical Management of Increased ICP
1. Hyperventilation
Intervene with caution
Brief periods with acute neurologic deterioration to a PaCO2 of 30 - 35
mmHg
Risk of exacerbating cerebral ischemia
If prolonged HPV to PaCO2 of 25 - 30 mmHg is necessary, consider
SjvO2 for monitoring of CBF to detect cerebral ischemia
2. Osmotic Diuretics
Mannitol is most commonly used
Increases serum osmolality causing a shift of fluid from brain to
intravascular space
Hold for serum osmolality of greater than or equal to 320 mOsm/kg
May create a reverse osmotic shift if used in large amounts or by
continuous infusion
3. Diuretics
Lasix is an example
Effective doses range from 10 - 20 mg IV q6h
Creates a diuresis that pulls fluid from the brain
Watch for electrolyte imbalances
May alternate with Mannitol
Should be used based on Pulmonary Artery catheter data
4. Glucocorticoids
Decadron is an example
There have been no randomized studies that show a benefit with the use of
steroids except for brain tumor edema
5. Maintenance of Body Temperature
 Fever increases the brains metabolic rate and cerebral oxygen
consumption
Maintain normal body temperature with acetaminophen and/or
cooling blankets
Do not allow patient to shiver
Increases metabolic rate and cerebral oxygen consumption
Therapeutic Hypothermia
Cooling of the body to 36o
Neuroprotective
Stabilizes blood-brain barrier
Prevents cell death
Decreases metabolic rate
Decreases CO2 and lactate buildup
May prevent loss of cerebral autoregulation
Potential Complications of Therapeutic Hypothermia
Hypokalemia
Bradycardia
Decreased stroke volume
Decreased contractility
Tachypnea
Atelectasis, pneumonia, ARDS
Infection
Hyperemia and cerebral edema during rewarming
Nephrogenic diabetes insipidus
6. Sedatives
Benzodiazepines
Diazepam (Valium)
Midazolam (Versed)
Lorazepam (Ativan)
Propofol (Diprivan)
7. Neuromuscular Blocking Agents (NMB)
Pancuronium (Pavulon)
Vecuronium (Norcuron)
Cisatracurium (Nimbex)
Prevents IICP from coughing, agitation
Facilitates ventilation
Unable to perform a neurological assessment
Use with sedation and analgesia
Monitor level of paralysis with Peripheral Nerve Stimulator (PNS) for
Train of Four (TOF) response
TOF response goal: 1 - 2 twitches out of possible total of 4 twitches (1-
2/4)
8. Barbiturate Therapy
Pentobarbital is most commonly used
 High dose barbiturate therapy should be considered in patients with
increased intracranial pressure refractory to maximal medical and surgical
ICP reduction
Decreases metabolic rate
Decreases cerebral oxygen needs
Decreases EEG activity
Hypotension common secondary to peripheral vasodilation and mild
myocardial depression
K. Operative Interventions
1. Craniotomy
2. Removal of mass
3. Evacuation of CSF, blood
L. Nutritional Support
1. A head injured patient may require up to 80% more nutrition than a healthy
individual
2. Preferred method is enteral; if contraindicated, consider parental
M. Anticonvulsants
1. Seizures will dramatically increase ICP
2. Anticonvulsants dramatically decrease early seizures (within 7 days of injury)
but have little impact on late seizures (greater than 7 days after injury)
3. Dilantin (phenytoin) and Tegretol (carbamazepine) recommended
4. Not routinely used prophylactically

II. Neuro trauma: Traumatic Brain Injury

A. Definition
1. Any injury to scalp, skull or parenchyma
2. Classified based on GCS
a. Mild: GCS = 13-15
b. Moderate: GCS = 9-12
c. Severe: GCS = 3-8
B. Mechanism of injury

1. Deformation 2. Acceleration-Deceleration 3. Rotational

C. Scalp and skull injuries
1. Scalp injuries:
a. Extensive vascularity and poor contractility of vessels
b. Diagnosis made on physical exam
c. Treatment dependent on severity and mechanism of wound
2. Fractures:
a. Observation or surgery depending on degree of injury and type of
fracture
b. Basilar skull fractures
 1). Specific associated signs
a. Raccoons eyes (Anterior fossa)
b. Battles sign (Middle and Posterior fossa)
c. Ottorhea
d. Rhinorrhea
2). Diagnosis and treatment
a. CT poor for detecting
b. Plain skull x-rays and clinical criteria better
c. Treatment of fracture itself not necessary
d. Treatment of potential complications
D. Parenchymal injuries
1. Concussion
a. Transient, temporary neurogenic dysfunction without parenchymal
abnormality
b. Signs and symptoms vary in time and sequelae
c. Treatment
CT brain recommended
Observation
2. Contusion
a. Bruising of the surface of the brain
b. Signs and symptoms dependent on size and associated edema
c. Treatment : Dependent on degree of abnormality
1. CT brain
2. Observation vs. admit
3. Subdural hematoma
a. Collection of blood in the subdural space
b. Cause: venous bleeding from tearing of bridging veins
c. Diagnosis and treatment: depend on size, location symptoms
1. Diagnosis by non-contrast CT scan
2. Surgery (burr holes vs. craniotomy)
4. Epidural hematoma
a. Bleeding into the potential space between the inner periosteum and the
dura mater
b. Presentation
1. Brief LOC
2. Lucid period followed by rapid neurologic deterioration
3. High index of suspicion following blows to tempoparietal area
(middle meningeal artery)
c. Diagnosis and treatment
1. Diagnosis by non-contrast CT scan
2. Usually emergent surgical intervention is necessary
5. Intracerebral hematoma
a. Hemorrhage occurs in the parenchyma
b. Signs and symptoms related to mass effect
c. Diagnosis and treatment:
1). CT scan
 2). Surgical intervention may be necessary
3). Associated with poor outcomes and mortality
6. Penetrating injury
a. Missile injuries
b. Impalement injuries

III. Neuro Infections

A. Guillian-Barr Syndrome
1. Acute inflammatory polyneuropathy
a. Autoimmune response to a viral infection
b. Destruction of myelin sheath
c. Pt hx significant for acute infection (usually URI) within two
weeks of onset of GBS
2. Rapidly progressive motor loss
a. ascending and symmetrical
3. Autonomic dysfunction
a. Cardiac arrhythmias/BP fluctuations
b. Paralytic ileus/Urinary retention
c. SIADH
4. Diagnosis based on
a. Patient hx & Presentation
b. LP/EMG
5. Treatment
a. Plasmaphoresis
b. Respiratory support
c. Supportive therapy
B. Meningitis: Inflammation of the meninges
1. Viral
a. Not usually fatal
b. Occurs more often in children
2. Bacterial
c. Meningococcal meningitis:
1. Neisseria meningitides or streptococcus pneumoniae
2. Highest incidence in children and young adults
3. Rapid circulatory collapse due to overwhelming septicemia
4. Requires treatment of close contacts and healthcare personnel
3. Signs and symptoms
a. Adult: HA, fever, change in LOC, nuchal rigidity
1. Meningeal irritation: check Kernigs and Brudzinskis signs
Brudzinski's sign: involuntary flexion of the hip and knee
when the neck is passively flexed
Kernigs sign: leg bent at hip and knee at 90 degree angle;
extension of knee is painful. Patient will demonstrate
resistance.
 Brudzinskis sign Kernigs sign
b. Child: Fever, vomiting, bulging fontanelles, crying
4. Diagnosis and treatment
a. Dx made based on hx and LP findings
b. Early recognition and isolation
c. Organism specific antibiotic therapy for bacterial meningitis
d. Symptomatic and supportive care for viral meningitis
C. Encephalitis: inflammation of the brain caused by viruses, bacteria, fungi or parasites
1. Arthropod-borne viruses (West Nile)
a. Prevention!
b. Treatment supportive
2. Herpes Simplex
a. Acute onset/flu-like symptoms
b. Poor prognosis if treatment not initiated before coma
3. Treatment
a. Medical vs. Surgical
Dependent on pt condition, cause of infection, location of lesion
b. Steroids for cerebral edema
c. Control of ICP
d. Antibiotics or anti-parasitics
D. Encephalopathy
1. Hypoxic-ischemic (anoxic)
a. Cardiac arrest
b. Exsanguination
c. Drop in pO2
2. Metabolic
a. Hepatic/Renal failure
b. Hypo/hyperglycemia
c. Sepsis

Certification Questions
1. Mr. Jones is in the intensive care unit following a motor vehicle crash. He is oriented to
person, place, and time; can move all extremities; and follows commands. His pulse is 75
beats/min, his blood pressure is 120/70, and his respirations are 18 breaths/min and regular.
Which of the following is the earliest indicator that Mr. Jones' intracranial pressure is
increasing?
A. He exhibits decorticate posturing
B. He is oriented to person only
C. His blood pressure is 130/60 and his pulse is 58 beats/min
D. His respirations are 10 per minute and irregular
2. Which of the following nursing interventions will assist in preventing increased ICP in the
patient who has a head injury?
A. Draining a ventriculostomy whenever the ICP rises above 15 mm Hg
B. Providing rest periods between interventions
C. Trendelenburg's position with neck in alignment
D. Using aseptic technique when changing the ICP dressing

3. Mr. Jones is in the intensive care unit following a motor vehicle crash. He is oriented to
person, place, and time; can move all extremities; and follows commands. His pulse is 75 bpm,
his blood pressure is 120/70, and his respirations are 18 breaths/min and regular. Which of the
following is the earliest indicator that Mr. Jones' intracranial pressure is increasing?
A. He exhibits decorticate posturing
B. He is oriented to person only
C. His blood pressure is 130/60 and his pulse is 58 beats/min
D. His respirations are 10 per minute and irregular

4. A patient has survived a severe traumatic brain injury with a basilar skull fracture but has now
developed an elevated temperature. Although the nurses plan for managing fever in this patient
population will be multifactorial, the most important aspect will center on identifying:
A. Deep vein thrombosis, a frequently neglected complication of immobility
B. Meningitis, a potential complication of basilar skull fractures
C. Hypothalamic dysfunction or storming, a potentially lethal febrile syndrome after
head trauma
D. Foreign bodies still embedded in the skull base, a common course of infection

5. A patient is admitted to the ICU for neurologic monitoring, after sustaining a linear left
temporal skill fracture in a motor vehicle collision. The EMTs reported a transient loss of
consciousness at the scene. Within 2 hours of admission, the patients neurological status
deteriorates. The nurse suspects the patient has developed a:
A. Epidural Hemorrhage
B. Subdural hemorrhage
C. Subarachnoid hemorrhage
D. Intracerebral hemorrhage

6. During an initial neurologic assessment, the nurse finds that the patient has a positive
Brudzinskis sign and a positive Kernigs sign. Otherwise, the patients assessment is nonfocal.
Since the lumbar puncture performed earlier shows high protein and low glucose in the CSF, the
nurses most appropriate action at this time is to:
A. Prepare the patient for brain MRI to rule out mass lesion
B. Arrange for administration of plasmaphoresis
C. Prepare to administer IV antibiotics
D. Prepare the patient for a repeat LP to withdraw accumulating CSF
Bibliography

Albano, C., Comandante, L., and Nolan, S. (2005). Innovations in the Management of Cerebral
Injury. Critical Care Nurse Quarterly 28(2) pp. 135-149.

Alspach, J.G. (Ed.). (2008). AACN Certification and Core Review for High Acuity and Critical
Care. St. Louis: Saunders Elsevier

Alspach, J.G. (Ed.). (2006) American Association of Critical Care Nurses Core Curriculum for
Critical Care Nursing (6th ed.). Phila: W.B. Saunders Company.

Arbour, R. (2004). Intracranial Hypertension: Monitoring and Nursing Assessment. Critical

Care Nurse 24(5) pp. 19-33

Dennison, R.F. (2007). Pass CCRN! (3nd Ed) St. Louis: Moseby Saunders

Mcilvoy, L.H. (2005). The Effect of Hypothermia and Hyperthermia on Acute Brain Injury.
AACN Clinical Issues 16(4). Pp. 488-500.

Sole, M.L.; Klein, D.G.; and Moseley, M.J. (2005). Introduction to Critical Care Nursing, 4th
Edition. St. Louis: Elsevier Saunders

Urden, L. D.; Stacy, K. M.; and Lough, M. E. (2006) Thelans Critical Care Nursing: Diagnosis
and Management, 5th ed. St. Louis: Mosby Elsevier.

Wright, J.E. (2005) Therapeutic Hypothermia in Traumatic Brain Injury. Critical Care Nurse
Quarterly 28(2) pp. 150-