Neuro Lecture Flashcards
Elements of a focused neuro assessment
Purpose
Does a neuro assessment need to be done on a non-neuro patient?
Neuro exam
Categorized as 5 distinct elements: Level of consciousness, Motor function, Pupillary function, Respiratory function, Vital signs
Elements of a focused neuro assessment
Determine baseline status of the patient - where they are; need know to see if deviating from it
Identify changes from baseline
Identify life-threatening changes
Sudden neuro changes are bad
Purpose
Yes see if deviating from it
Does a neuro assessment need to be done on a non-neuro patient?
7 levels of consciousness: - not know but just know what means
What are we assessing?
What part of the brain is involved?
How does the nurse assess LOC?
LOC
Pt responds immediately to minimal external stimuli
Alert - 7 levels of consciousness: - not know but just know what means
Pt is disoriented to time or place but usually oriented to person, with impaired judgment and decision making and decreased attention span
Confused - 7 levels of consciousness: - not know but just know what means
Pt is disoriented to time, place, and person, with loss of contact with reality and often has auditory or visual hallucinations
Delirious - 7 levels of consciousness: - not know but just know what means
Pt displays a state of drowsiness or inaction in which pt needs increased stimulus to be awakened
Lethargic - 7 levels of consciousness: - not know but just know what means
Pt displays dull difference to external stimuli, and response is minimally maintained
Questions are answered with a minimal response
Obtunded - 7 levels of consciousness: - not know but just know what means
Pt can be aroused only by vigorous and continuous external stimuli
Motor response is often withdrawal or localizing to stimulus
Stuporous - 7 levels of consciousness: - not know but just know what means
Vigorous stimulation fails to produce any voluntary neural response
Comatose - 7 levels of consciousness: - not know but just know what means
Awake; mentating well; we say alert and oriented
Answer: Brainstem and cortex
Communication between: thalamus - in there reticular activating sys links them together
Low LOC - next thought is: do we need take measures on how keep safe, oriented enough to use the call light; if not - we need to provide the safe environment, move closer to nurses station, hourly rounding; no restraints
What are we assessing?
Alert and arousal - assessing the brainstem - where wakefullness is - awake and alert - brainstem in tack
Oriented - higher func - cortex/cerebrum
Both have to be operating to be alerted and oriented
Can be oriented and not alert
What part of the brain is involved?
GCS
How does the nurse assess LOC?
Looking at alert and oriented status and quantifying it
Is the Glasgow Coma Scale (GCS) a complete neuro exam?
Category:
Glasgow coma scale
No
Tell if have higher level functioning and if brainstem somewhat in tack
Not complete assessment of each
Is the Glasgow Coma Scale (GCS) a complete neuro exam?
eye opening - brainstem; arousable, awakable, alert - when walk in room, open eyes and acknowledge in room
Verbal response - higher func; motor and sensory strip in brain
Best motor response - higher func; motor and sensory strip in brain
Category:
4
Spontaneous: eyes open spontaneously without stimulation
3
To speech: eyes open with verbal stimulation but not necessarily to command
2
To pain: eyes open with noxious stimuli
1
None: no eye opening regardless of stimulation
eye opening - brainstem; arousable, awakable, alert - when walk in room, open eyes and acknowledge in room
5
Oriented: accurate information about person, place, time, reason for hospitalization and personal data
4
Confused: answers not appropriate to question but use of language is correct
3
Inappropriate words: disorganized, random speech, no sustained conversation
2
Incomprehensible sounds: moans, groans, and incomprehensible mumbles
1
None: no verbalization despite stimatulation
Verbal response - higher func; motor and sensory strip in brain
6
Obeys commands: performs simple tasks on command; able to repeat performance
5
Localizes to pain: organized attempt to localize and remove painful stimuli
4
Withdraws from pain: withdraws extremity from source of painful stimuli
3
Abnormal flexion: decorticate posturing spontaneously or in response to noxious stimuli
2
Extension: decerebrate posturing spontaneously or in response to noxious stimuli
1
None: no response to noxious stimuli, flaccid
Best motor response - higher func; motor and sensory strip in brain
Muscle size and tone (size, shape)
Muscle Strength
Highest movement score charted
Motor responses (used when pt. cannot follow commands)
Superficial reflexes (table 22.2)
Deep tendon
Motor func
Opposition to passive movement flaccid, hypotonia, hypertonia, spasticity, rigidity.
Asymmetry does not happen until much later when atrophy happens
Motor func
Opposition to passive movement flaccid, hypotonia, hypertonia, spasticity, rigidity.
Asymmetry does not happen until much later when atrophy happens
Muscle size and tone (size, shape)
Movements against resistance
Pronator drift, lift legs
Push and pull
Muscle Strength
Classifications of abnormal motor function Reflexes
Spontaneous
Localizations
Withdrawal
Decortication
Decerebration
Flaccid
Motor responses (used when pt. cannot follow commands)
Occurs without regard to external stimuli and may not occur by request
Do what is requested of them
Spontaneous
Occurs when the extremity opposite the extremity receiving pain crosses midline in an attempt to remove the noxious stimulus from the affected limb
Localizations
Occurs when the extremity receiving the painful stimulus flexes normally in an attempt to avoid the noxious stimulus
Withdrawal
Abnormal flexion response that may occur spontaneously or in response to noxious stimuli
Decortication
Abnormal extension response that may occur spontaneously or in response to noxious stimuli
Decerebration
No response to painful stimuli
Flaccid
Stimulating the cutaneous receptors (skin, cornea, mucus membrane)
Corneal reflex (V, VII) and pharyngeal reflex (IX, X)
Looking at brainstem with cranial nerves
Focused assessment - look at cranial nerves
Superficial reflexes (table 22.2)
Hammer
Func - spinal column - SC - not in brain
Deep tendon
Group into Swallowing and eye movement
Cranial nerves come off brain stem and innervate whatever need; sx on same side; ipsilateral (innervate on same side) - not contralateral (opp sides) like the cortex
All cranial nerves ipsilateral
Eye movement
Swallowing
TEST on cranial nerves - name and number
IV - tip of the nose
VI - horizontal to ear
III - everything else
Eye movement
Anything affects oropharyngeal coordination and moving fluid bolus from front to back mouth - not adjoining to the esophagus
When check uvula - uneven - something wrong with cranial nerves
V - not move food bolus around
VII
IX
X
XII
Swallowing
Assessment
Oculo-cephalic reflex (AKA Doll’s eyes)
Pupillary func
Pupil size and shape
Cranial nerve III (constricts pupil)
Pupil reaction to light
Cranial nerve II
Assessment of eye movements.
Cranial nerves: III, IV, VI
Assessment
Checking cranial nerves and eyeballs to see if functioning right
Looking at III (horizontal) and VI - seeing if intact because unable to follow finger
Lay flat
Eyeballs still looking at ceiling - Move head swiftly right and eyes move left - brainstem in tact - + Doll’s eyes reflex
Move head and eyes stay - eyes in fixed position - abnormal - something wrong with brainstem at 3 and 6 level
Not done if conscious - can overcome reflex and move eyes whatever direction
The nurse rapidly turns the patient’s head from side to side. The eyes move laterally in the opposite direction. Normal or Abnormal?
Normal
Your patient has an absence of doll’s eyes reflex. What part of the brain is not functioning properly?
Brainstem
A positive Dolls eye’s reflex like the gag reflex and blink reflex. Positive is good
Can the doll’s eyes reflex be tested in a conscious patient?
No. Unconscious only
Oculo-cephalic reflex (AKA Doll’s eyes)
Low in brainstem - probs this low - Lot pressure on brainstem
Respiratory pattern (Abnormal respiratory patterns Fig. 22.3)
Evaluation of airway status
Cheyne-Stokes breathing –
Central neurogenic breathing -
Ataxic respiration -
Cluster breathing
Apneustic breathing
Abnormal breathing with brainstem - ventilator or O2 not make it better - not P/Q issie - prob with brainstem - get out acidosis - cluster and nurogenoc: notify PCP if new
Respiratory Function
Even, labored/nonlabored, eupneic, tachypneic. . .
A mechanical ventilator will not prevent or treat abnormal respiratory patterns that originate in the brainstem.
Should include an assessment of gas exchange
SaO2 & Co2 levels
Respiratory pattern (Abnormal respiratory patterns Fig. 22.3)
Maintaining airway, secretion control
Evaluation of airway status
(Rhythmic crescendo and decrescendo of rate and depth of respiration with brief periods of apnea. ) Usually seen with bilateral deep cerebral lesions and cerebellar lesions, not the brainstem.
See lot with metabolic issues
Primary issue: metabolic or something with cortex
Only one in cortex
Use ventilator to get out of acidosis state
Cheyne-Stokes breathing –
brainstem (Very deep, very rapid respirations with no apneic periods.)
40s-50s RR and very deep
Ventilator not fix
ABG - more alkalosis - blowing lot off
Central neurogenic breathing -
brainstem (Irregular, random pattern of deep and shallow respiration with irregular apneic periods.).
All over place
No pattern
Ventilator not fix
See with herniation
Ataxic respiration -
See with herniation
Ventilator not fix
Clusters of irregular, gasping respirations separated by long periods of apnea
Usually seen in lesions of lower pons or upper medulla
Brainstem
Cluster breathing
Ventilator not fix
Prolonged inspiratory and/or expiratory pause of 2-3 seconds
Usually seen in lesions of middle to lower pons
Brainstem
Apneustic breathing
Blood Pressure
Heart rate & rhythm
Cushing’s triad:
Vital Signs
A common manifestation of intracranial injury is systemic hypertension.
Blood Pressure
X - vagus nerve - controls HR and rhythm
Will have an arrythmia
Heart rate & rhythm
systolic hypertension, bradycardia, abnormal respirations (bradypnea)
Indicator for increased ICP and intracranial HTN - close to herniation - so much pressure in skull and brain pushed out through foramen magnum
Cushing’s triad:
Parts of the Neuro exam include: Level of consciousness, Motor function, Pupillary function, Respiratory function, Vital signs. - not matter order; all parts must be done
Categories of Consciousness: Box 22.2
Baseline neuro assessment is needed to determine if a patient has a change in neuro status. - NECESSARY; first thing do; know if change
Changes in neuro status should be assessed the underlying cause - any sudden change = EMERGENCY; ie - not mean drastic - just means happens fast; just going to get worse unless treated
Sudden neuro changes are a priority concern.
The neuro exam is a clinical assessment tool that is used to determine what specific parts of the CNS are affected by damage or disease.
Key points
Definition: absence of both wakefulness and awareness
What part of the neuro assessment is this?
LOC
Causes
Lab values for DI & SIADH: I will use the same lab values that were used when you first learned these concepts in AH2. They are also found in the Endocrine Alterations chapter.
Hepatic encephalopathy:
Causes of Coma
Coma
Anything can cause it
Structural or surgical
Metabolic (intoxication) or medical
Causes
Intoxication
Sepsis
Hypo/hyperglycemia
Meningitis
Overdose
What labs (and lab values) are associated with metabolic causes? - Metabolic (intoxication) or medical
Blood alcohol labs
Unconscious: 4-450; chronic alcoholics 800 - Liver exercised
At a blood alcohol concentration of 450 grams per 100 ml (0.45 percent) or above, a person is likely to become comatose and die from alcohol intoxication.
ALT - 15-65 u/L
ASF - 12-37 u/L
Blood alcohol - 0
Intoxication
Lactate - comatose about 2-3
Lactate - <2mmol/L
Sepsis doesn’t always cause coma. It’s when the sepsis is in the later stages of the patient is in septic shock that coma will occur. Lactate is an important source of energy, particularly during starvation/hypoxia. When the patient is starved or hypoxic lactate is overproduced during anaerobic glycolysis and the lactate levels rise. Generally, a lactate level greater than 2 mmol/L is associated with coma.
Sepsis
BG levels
Machines say high or low - need lab draw
Serum glucose level < 50 mg/dL or > 300 mg/dL will result in coma.
Low - give glucose
Hypo/hyperglycemia
the presence of bacteria
Enough to put in comatose state
Look at lumbar puncture
Look at CSF - is bacterial: cloudy, glucose low
Viral - clear, glucose normal
Meningitis
Substance +
Overdose
An ammonia level higher than 100 µmol/L (170 µg/dL) is diagnostic for hepatic encephalopathy. In this disease process, an elevated Ammonia level does not cause coma. Rather it’s the brain’s response to the elevated ammonia that causes coma. The ammonia crosses the blood brain barrier where it is converted to glutamine. Once the glutamine levels increase in the brain cell, it causes an osmotic shift of extracellular fluid to the intracellular space causing cerebral edema which then causes intracranial hypertension. It’s intracranial hypertension that causes coma.
Hepatic encephalopathy:
Trauma
Epidural hematoma
Subdural hematoma
Diffuse axonal injury
Brain contusion
Intracerebral hemorrhage
Subarachnoid hemorrhage
Posterior fossa hemorrhage
Supratentorial hemorrhage
Hydrocephalus
Ischemic stroke
Tumor
Other causes
Structural or surgical coma - Causes of Coma
Infection
Meningitis
Encephalitis
Metabolic encephalopathy
Metabolic conditions
hypo/hyperglycemia
Hyperosmolar states
Uremia
Hepatic encephalopathy
Hyertensive encephalopathy
Hypoxic encephalopathy
Hyponatremia
Hypercalcemia
Myxedema
Intoxication
Opioid overdose
Alcohol
Poisonings
Psychogenic causes
Metabolic or medical coma - Causes of Coma
Catch all dx
Coma established by assessing LOC
Brainstem and cortex not functioning - usually couple other dx with it
Not participate in neuro assessment
H & P
Assessment: A detailed serial neurologic examinations are essential for all patients in coma
Coma assessment and dx
LOC - not arousable and not answering questions; no verbal response
Look at H&P - see if have comorbidities - issues with substance abuse; diabetic; chronic alcohol abuse
Pupil size & reaction to light
Extraocular eye movements - Doll’s eyes; oculo-cephalic reflex
Motor response to pain - pressure; need see purposeful withdrawal; noxious stimuli - not just pain, sternal rubs, smelly salts
Breathing pattern (provides clues to the origin: structural vs. metabolic: Cheyne-Stoke’s - may be DKA - not a head issue)
Assessment: A detailed serial neurologic examinations are essential for all patients in coma
Two main causes: structural (either traumatic or surgery) and metabolic (alcohol, DKA)
Deepest state of unconsciousness
Medical management: identification and treatment of underlying cause and support of vital functions
Nursing management: supporting body functions, watching for complications, providing comfort and emotional support, initiating rehabilitation measures (consulted early - esp if have catastrophic injuries if have bone flap out where need high level of specialized of care), and educating patient and family - understand appear more sick and sx more profound for few days after until swelling going down
Coma - Summary
Two types of surgery
Preoperative education / Postoperative Care
Post-op
Craniotomy
Transcranial - peel skin back and causes soft tissue damage on face
Transsphenoidal - through the nose or under the lip - issues with bottom of brain; often pit gland
Two types of surgery
General
Transcranial specific
Transsphenoidal specific
Preoperative education / Postoperative Care
Facial/eye swelling regardless of where surgery is & ecchymosis (bruising)
Avoid activities that increase intracranial pressure
General
Shaved head
Bulky turbin dressing
Transcranial specific
Nasal packing - full; heavy pack
Avoidance of coughing/blowing nose - lot edu - beyond ICP
Break the bone to get in there to work and use bone glue and patch it up and until bone grows in blow out bone with brain - fragile
Transsphenoidal specific
Medical management
Nursing management: focused on preserving cerebral perfusion
Post-op
Intracranial hypertension
Surgical hemorrhage
Fluid imbalance
Cerebrospinal fluid leak
Medical management
Peaks at 48 -72 hours - intercerebral edema (poking around - will swell)
CSF drainage, pt. positioning, and steroids
Intracranial hypertension
Breaking lot caps
Soft tissue hematoma from skull - where void - fill with void and Get hemorrhagic convergance
Transcranial – presents as increased ICP
Transsphenoidal – presents as persistent postnasal drip or excessive swallowing. Loss of bitemporal vision. Can present as increased intracranial pressure.
Surgical hemorrhage
Related antidiuretic hormone
Fluid imbalance
Related to an opening in the subarachnoid space: clear fluid (+) glucose
Transsphenoidal - runny nose
Transcranial - clearish fluid: send down to see what going on and what it is
Cerebrospinal fluid leak
Need maintain ICP
Positioning
Fluid management
Avoidance of vomiting - increases intracranial pressure - increases intrathoracic pressure, get antiemetics as soon as feel nauseated
Avoidance of fever - increases metabolic demand - tylenol and cooling gel pads/blankets
Comfort & emotional support
Promote arterial oxygenation (airway & breathing) - brain not tolerate low O2 states; brain not forgiving; maintain oxygenation and ventilation
Early on: Avoid increasing metabolic demand (htn, anxiety, pain, elevated temp, external stimuli…)
Assess for complications: infection, corneal abrasions, pressure ulcers, injuries
Early mobilization should be avoided (increases metabolic demand) - do not push them if cannot tolerate
Nursing management: focused on preserving cerebral perfusion
↑ HOB - can go flat - depends on how responsive to position change
Head in neutral, midline position (affects venous return)
Positioning
I & O - DI (pee too much), SIADH (no pee; retention)
Fluid restriction
Fluid management
Limit visitation if ICP increases until less responsive
Sustained increased ICP
Want to decrease stimulation from TV and people
May administer sedation
PRN P.O./IV benzodiazepines - IV benzos for anxiety and fam leaves
Titrate continuous IV sedation
Early on: Avoid increasing metabolic demand (htn, anxiety, pain, elevated temp, external stimuli…)
On a continuum - both probs with LOC
Early signs of increased ICP:
Late signs of increased ICP:
Interventions for preventing/treating increased ICP.
Increased ICP
LOC: Loss of insight, loss of recent memory, restlessness, irritable, uncooperative, requires more stimulation to get the same response, speechless distinct, sudden quietness
More confusion
Sleepy, shake to wake up; talk to wake up
Less severe
New weakness in extremities
Pupils: Sluggish to light, usually unilateral, Ipsilateral to lesion, papilledema or bulging of the optic discs, blurred vision.
Vital signs: Occasionally tachycardic, Occasional hypertensive swings
Early signs of increased ICP:
LOC: Arousable only with deep pain, unarousable
Obtunded
Not waking up
Noxious stimuli to wake them up
More severe
Flaccid in extremities - profound weakness; not able hold arm
Motor: dense hemiparesis (not move it), abnormal flexion (GCS - decerberate or decorticate - can be onesided posturing), abnormal extension, no response (flaccidity preliminary to death)
Late signs of increased ICP:
Pt. positioning - head up and midline
Forced gaze - sand bags on side of head to keep straight
Controlled hyperventilation - ABG back to normal; not to point where get alkalosis because causes vasodilation because takes up space in skull; controlled = get to normal spot
Temperature Control
Blood pressure control - will let run higher so higher CPP so more oxygenated blood through the head - higher presssure to keep perfused; ischemic strokes: not qualify for tPA - stay high - to get blood on other side of brain; after surgery - not do so: cause hemorrhagic conversion - will bleed
Interventions for preventing/treating increased ICP.
s&s and nursing interventions same - pt sicker
Normal ICP: <15 mm Hg
Elevated ICP: 15 to 19 mm Hg
Moderately elevated ICP: 20 to 30 mm Hg
Severely elevated ICP: >40
Higher go - get into HTN
What occupies the intracranial space?
Intracranial hypertension
Brain
CSF
Intracranial blood
How does the body compensate if one of the above increases?
What are some causes of increased ICP/intracranial hypertension?
What occupies the intracranial space?
Always trying to compensate - lot blood in vasculature - affecting reabsorption - try compensate to point - do CSF
How does the body compensate if one of the above increases?
Bleeding
Hydrocephalus issues
Aneurysm
Slow growing tumors that are gradual
What are some causes of increased ICP/intracranial hypertension?
Positioning
Fluid management
Avoidance of vomiting - increases intracranial pressure - increases intrathoracic pressure, get antiemetics as soon as feel nauseated
Avoidance of fever - increases metabolic demand - tylenol and cooling gel pads/blankets
Comfort & emotional support
Promote arterial oxygenation (airway & breathing) - not forgiving; maintain oxygenation and ventilation
Avoid increasing metabolic demand (htn, anxiety, pain, elevated temp, external stimuli…)
Assess for complications: infection, corneal abrasions, pressure ulcers, injuries
Early mobilization should be avoided (increases metabolic demand) - do not push them
Normothermic
Turn off TV
Decrease BP
Seizure control
CSF drainage
Interventions to manage intracranial pressure (ICP)
↑ HOB - can go flat - depends on how responsive to position change
Head in neutral, midline position (affects venous return)
Positioning
I & O - DI (pee too much), SIADH (no pee)
Fluid restriction - fluid balance
Fluid management
Limit visitation if ICP increases
Sustained increased ICP
May administer sedation
PRN P.O./IV benzodiazepines - IV benzos for anxiety - on standing orders
Titrate continuous IV sedation
Avoid increasing metabolic demand (htn, anxiety, pain, elevated temp, external stimuli…)
Phosphenotwain
Seizure prophylaxis until blood reabsorped
Seizure control
EVD - distal tip in ventricles of catheter - off center - medial vein - distal tip sits there and drains it off
Should be clear
For trauma and post-op - pinky-red
Drain slowly
Do not flush
mmHg/cmH2O
CSF drainage
LOC
Loss of insight (confusion)
Loss of recent memory
Restless, irritable, uncooperative
Requires more stimulation to get same response
Speech less distinct
Sudden quietness
Other
Vomiting
Headache
Pupils
Sluggish to light response
Usually unilateral
Ipsilateral to lesion
Papilledema or bulging of optic discs
Blurred vision
Vital signs
Occasionally tachycardic
Occasional hypertensive swings
Early signs of increased ICP
LOC
Arousable only with deep pain
Unarousable
Motor function
Dense hemiparesis
Decerebrate posturing (abnormal extension)
Decorticate posturing (abnormal flexion)
No response (flaccidity preliminary to death)
Vital signs
Cushing triad (bradycardia, systolic hypertension, and bradypnea)
Late signs of increased ICP
Straw colored - blood in it
Not want pinky, red
Very few are clear
Ruptured aneurysm - catastrophic event
Drain:
After intracranial HTN
Nowhere else for brain to swell - completely occupied cranial vault - excruted out foramen magnum - once out - not pushed back in - see midline shift
Goal is to prevent herniation
Where something should not be
Know early, late, uncal, central
Definition: The displacement of brain structures resulting in a sequence of neurological signs and symptoms related to compression of brain structures and compromised blood flow
Herniation is a process that can be reversed, but the time for doing so is limited
Two main categories
Uncal -
Central Herniation
Herniation syndromes
Supratentorial: uncal, central
Infratentorial:
Two main categories
Most common
Something happening up in cerebrum
Usually more temporal - subdural, hemorrhage, tumor
Dura up around and latched in on self between cerebellum and cortex
Causing cortex to be squished out of the way
Enough pressure put on brain tissue that goes down and squishes the brainstem
Subdural hematoma
Sx from brainstem and cortex
Brainstem sx - related to cranial nerve III getting squished
Nothing out foramen magnum
Recoverable
Unilateral, expanding mass, increases ICP
Lateral displacement pushes the uncus (innermost part of temporal lobe) over the edge of the tentorium (second-largest dural reflection that extends over the posterior cranial fossa. It separates the occipital and temporal lobes of the cerebrum from the underlying cerebellum and brainstem, and divides the cranial cavity into supratentorial and infratentorial spaces) putting pressure on the midbrain
Early symptoms
Late symptoms
Everything is singlular/one sided
One eyeball affected
Ipsilateral to lesion because cranial nerve III (eye movement and pupil affected) squished
Uncal -
Decreased LOC - messing with brainstem
Ipsilateral pupil dilation - on affected side
Disconjugate doll’s eye - one eyeballs not moving because cranial nerve III messed up
Cheyne-Stokes respirations
Contralateral motor weakness - on motor strip
Early symptoms - Uncal -
Be more obtunded
Central neurogenic hyperventilation - Abnormal respiratory patterns
Ipsilateral fixed and dilated pupil
Disconjugate doll’s eye
Contralateral decorticate or decerebrate posturing - quickly
Late symptoms - Uncal -
Both eyeballs affected
Downward displacement of the hemispheres (temporal lobes), basal ganglia, and diencephalon through the tentorial notch that compresses the brainstem.
Clinical manifestations
Central Herniation
Decreased LOC
Small, reactive pupils
Respiratory changes & unstable vital signs
Abnormal decorticate posturing - both sides
The first phase of central herniation, the diencephalon (thalamus & hypothalamus) and the medial parts of both temporal lobes are forced through the tentorium cerebelli notch. In the early stage, which is reversable, the patient will have decreased LOC with difficulty concentrating, agitation and drowsiness. Pupils will be small (1-3mm) but reactive. Oculocephalic (dolls eye’s) will be intact. Patient’s respirations will change. Often, they will have deep sighs, yawns. The patient’s symptoms will progress if the cause of the central herniation is not identified and treated. The patient will become more difficult to arouse, localizing motor response to pain will disappear and the pt. will start posturing.
Early- Central Herniation
Coma - decompensate quickly
Fixed, dilated pupils
Respiratory arrest
Flaccidity
Cardiopulmonary arrest - code quickly
In the later stages of central herniation the midbrain & upper pons is affected. The motor tone is increased and the pt will have decerebrate posturing. The pupils will be irregular and fixed at the midline position. The pt will have abnormal respirations – hyperventilation. The symptoms will progress, and the pt. will become comatose (no spontaneous motor activity, not arousable), the pupils will be fixed and dilated, absence of oculocephalic (doll’s eyes) and will have ataxic respirations. When the pt. enters the late stage of central herniation the medulla is affected. The pt. will have generalized flaccidity, fixed and dilated pupils, absent oculocephalic reflex, ataxic respirations will progress to cardiopulmonary arrest.
Late - Central Herniation
Intracranial hypertension
s&s - more profound side of pressures
Measure with ICP
Big fan of intraventricular catheter and EVD
In PPT - that is level
Early sign of increased ICP is decrease in level of consciousness
ICP can be measured using ICP monitor
Medical and nursing management: reducing volume of one or more of components within intracranial vault
Herniation of intracerebral contents results in shifting of tissue from one brain compartment to another and places pressure on cerebral vessels and vital function centers of the brain; if unchecked, results in death
Pharmacologic management aimed at symptom control: seizures, cerebral oxygen demand, cerebral edema, blood pressure
Summary
