Neuro Lecture Flashcards by Kelsey Klipfel

Elements of a focused neuro assessment
Purpose
Does a neuro assessment need to be done on a non-neuro patient?

Neuro exam

How well did you know this?

Not at all

Perfectly

Categorized as 5 distinct elements: Level of consciousness, Motor function, Pupillary function, Respiratory function, Vital signs

Elements of a focused neuro assessment

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Yes see if deviating from it

Does a neuro assessment need to be done on a non-neuro patient?

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Pt responds immediately to minimal external stimuli

Alert - 7 levels of consciousness: - not know but just know what means

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Vigorous stimulation fails to produce any voluntary neural response

Comatose - 7 levels of consciousness: - not know but just know what means

How well did you know this?

Not at all

Perfectly

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?

How well did you know this?

Not at all

Perfectly

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?

How well did you know this?

Not at all

Perfectly

GCS

How does the nurse assess LOC?

How well did you know this?

Not at all

Perfectly

Looking at alert and oriented status and quantifying it
Is the Glasgow Coma Scale (GCS) a complete neuro exam?
Category:

Glasgow coma scale

How well did you know this?

Not at all

Perfectly

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?

How well did you know this?

Not at all

Perfectly

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:

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Opposition to passive movement flaccid, hypotonia, hypertonia, spasticity, rigidity.
Asymmetry does not happen until much later when atrophy happens

Motor func

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

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