Session Number 311 CCRN-PCCN-CMC REVIEW: NEURO PART 1

16 Pages·2013·0.21 MB·English

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

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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
Cushing’s 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 (Wernicke’s aphasia) – Comprehension
of speech impaired. Able to make words, but will
be nonsensical, rambling. Unable to identify
written words.
Expressive aphasia (Broca’s 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
Cushing’s 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
patient’s 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 PaCO of 30 - 35
2
mmHg
Risk of exacerbating cerebral ischemia
If prolonged HPV to PaCO of 25 - 30 mmHg is necessary, consider
2
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 brain’s 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 CO and lactate buildup
2
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