Transcript Increased Intracranial Pressure

The
Skull
The
brain’s
protector
THE SKULL
Made of 8 irregularly fused bones
Smooth on the outside, folds and ridges on the inner surface
The Cranial Vault
Foramen magnum
The Brain (80%)
Increased Brain Volume
 Mass
Cerebral Swelling
Blood (10%)
 Normally about 750cc of
circulating volume
 20% of the Cardiac Output
Increased Blood Volume
Hemorrhage
Vasodilatation
Cerebrospinal Fluid (10%)
Increased CSF Volume

Hydrocephalus
Intracranial Pressure (ICP)
 The pressure exerted by
the brain tissue,
intracranial blood, & CSF
Tough Mother
Dura Mater
 Double layered
 Inelastic, fibrous
membrane
 Holds the brain in place
Epidural Space
 Space that is directly above
the Dura
 Middle Meningeal Artery
is present here
Cerebral lobes
Frontal lobe
Movement
Impulses
Frontal lobe
Spoken Language
Personality
Parietal lobe
Sight Understanding
Touch Understanding
Parietal lobe
Distance and Position to Objects
Temporal lobe
Written Words
Hearing
Memory
Damage Causes Ipsilateral Movement
Pons
Mid Brain
Medulla Oblongata
 ABC’s First
 Quick History
 LOC
 Vital Signs
Down and
Dirty
 Pupils
 Early or Late?
 Early: restlessness, disorientation, lethargy
 Late: Increase BP, pupillary changes, seizures
 GLASGOW COMA SCALE
 Best Eye Opening
 Best Verbal Response
 Best Motor Response
Assessment
Best Eye Opening
Spontaneously-4
 To Verbal Command-3
 To Pain-2
 No Response-1

Best Verbal Response
Oriented, Converses-5
 Disoriented, Converses-4
 Inappropriate words-3
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Incomprehensible sounds-2

No Response-1
Best Motor Response
 Obeys Commands-6
 To Pain

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Localizes Pain-5
Flexion Withdrawal-4
Abnormal Flexion-3
Abnormal Extension-2
No Response-1
Glasgow Coma Scale
Pediatrics
 Verbal (2 to 5 years)
 Appropriate words or -5
 Inappropriate words-4
 Persistent cries and/or screams-3
Glasgow Coma Scale
Pediatrics
 Verbal (0 to 23 months)
 Smiles or coos appropriately-5
 Cries and consolable-4
 Persistent inappropriate crying
and / or screaming-3
Severity of Injury
 Mild
◦ GCS Score 14-15
 Moderate
◦ GSC Score 9-13
 Severe
◦ GCS Score 3-8
A desk scores a “3”
Loss of Consciousness
“A,E,I,O,U TIPS”
A
T
 Alcohol
E
 Trauma, toxicity, tumors,
thermoregulation
 Epilepsy
I
 Insulin (too much, too
P
I
little)
O
 Infections, ischemia
 Psychiatric, poisonings
S
 Oxygen (too much, too
little)
U
 Uremia or other
metabolic issues
 Stroke, syncope or other
neurologic /
cardiovascular causes
Babinski’s Reflex
 Present when stroking of Planter surface of foot causes
Flexing of great toe
 Fanning of other toes
 Normally present in children <2yo
 Presence in >2yo indicates problem in corticospinal tract
(nerve path spine to brain)

 Abnormal posturing is a late sign of
increasing ICP
 Decorticate
Abnormal flexion
 Decerebrate
 Abnormal extension

Meningeal Signs
 Nuchal rigidity
 Stiff neck, pain on flexion
 Photophobia
 Positive Brudzinski’s
 Involuntary flexion of knees/hips when neck
flexed
 Positive Kernig’s
 Unable to straighten leg when hip fully flexed in
supine patient
Increased Intracranial Pressure
Intracranial Pressure
 Intracranial pressure reflects
 Brain
 Cerebrospinal fluid
 Blood
 As intracranial pressure increases, cerebral perfusion
pressure decreases
 Leads to cerebral ischemia and hypoxia
 In a hypotensive patient, even a marginally elevated ICP
can be harmful
 Adequacy of cerebral perfusion pressure is most
important
Increased Intracranial Pressure
 Initially -intracranial volume increasesICP remains stable.
 System becomes less compliant, or less
able to tolerate increases in volume
 Later, intracranial volume cont’s to
increase, less compliance will be unable
to buffer the increases and ICP will rise
Increased Intracranial Pressure
Assessment
 Early picture of increased intracranial pressure (IICP)
 LOC
 Loss of insight
 Loss of recent memory
 Restless, irritable, uncooperative behavior
 Requires more stimulation to get same response
 Speech less distinct
 Sudden quietness in a very restless patient
Increased Intracranial Pressure
Early Increasing ICP
Motor function
 Usually contralateral to lesion
 Pronator drift
 Loss of one or more grades on the strength scale
 Increased tone
Increased Intracranial Pressure
 Early Increasing ICP
 Pupils
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
Sluggish to light response
Usually unilateral
Ipsilateral to lesion
Papilledema or bulging of optic discs
 Blurred vision
Increased Intracranial Pressure
 Early Increasing ICP
 Vital signs


Occasionally tachycardic
Occasional hypertensive swings
Increased Intracranial Pressure
 Late Increasing ICP
 LOC
Arousable only
with deep pain
 Unarousable
 Motor function
 Dense hemiparesis
 Abnormal flexion
 Abnormal
extension
 No response
(flaccidity
preliminary to
death)

 Abnormal posturing
is a late sign of
increasing ICP
 Decorticate
Abnormal flexion
 Decerebrate
 Abnormal extension

Increased Intracranial Pressure
Sign & SymptomsImpending Herniation
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Decreased LOC
Motor Dysfunctions
Pupillary abnormalities
Impaired Reflexes
Changes in Vital Signs
Irregular respirations
Increased Intracranial Pressure
Late Signs Increasing ICP
Vital signs
 Cushing’s triad
 Very late sign of increasing ICP, last ditch effort
to perfuse brain
 Elevated SBP
 Bradycardia
 Widening pulse pressure
Increased Intracranial Pressure
Interventions
 ABC’s
 Mechanically decrease ICP
 Oxygenate
 Osmotic Agents
Increased Intracranial Pressure
Osmotic Agents
 Mannitol:
 reduces ICP within 15 minutes with continued
effectiveness for 2-3 hours
 Monitor serum osmolarity
Increased Intracranial Pressure
Treatment of ICP
 Easiest to manipulate is
BP and CSF
 proper head alignment
 sedation
 Surgery
Goal
Keep
SBP>90
Traumatic Brain Injury
Injury to skull, brain,
or both that is of
enough magnitude to
interfere with normal
neurological function
Nearly 2 million people sustain
head injuries each year
70,000 die prior to hospitalization
TBI
Another 25,000 die following
hospitalization
90,000 people will
have significant
permanent
neurological
disabilities for the
rest of their lives
Traumatic Brain Injury
The peak age for neurotrama is 15 to 30
years of age
Causes of TBI
Motor Vehicle
25%
Falls
7%
Recreation
30%
Bicycles
10%
Motor Vehicle
Violence
5%
Violence
20%
Shaken Infant
Syndrome
3%
Concussion
 Transient impairment of neurological function caused
by a mechanical force
 Rapid acceleration-deceleration
 if repeated can produce a permanent deterioration in
intellect
 recent studies suggest long term impairment even with
“moderate”concussion
 “moderate” if loss of consciousness
Concussion
 Diagnosis
 CT scan
Rule out other injury
 Clinical picture
 History of injury

Concussion
 Interventions
 Assess neuro status
 Patient/Family education return to facility
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Change in LOC
Change in pupils
Projectile vomiting
Seizure
Inability to arouse
 Interventions
 Educate patient/family
 Post concussion syndrome
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
H/A
Dizziness (positional)
Tinnitus
Inability to concentrate
Personality change
Memory disturbances
 Interventions
 Educate patient/family

Post concussion syndrome
 Duration
 Days to years
 Social/occupational
 Difficulty school/work
Diastatic Skull Fractures
 Fracture along
suture line
 Often seen in
children
Depressed Skull Fracture
 A break in a cranial bone (or "crushed" portion of skull)
with depression of the bone in toward the brain
 May require surgical elevation
Compound
Skull
Fracture
A break in or loss of skin and splintering of the bone.
Basilar Skull
Fracture
 A Fracture that occurs somewhere in the Cranial
Vault
Basal Skull Fractures
Periorbital ecchymosis
(Raccoon sign)
Anterior fracture
Basal Skull fracture
Retroauricular
ecchymosis
(Battle’s sign)
--Posterior fracture
Blood behind tympanic
membrane
--Middle Fracture
Basilar Fractures cont’d
 If Basilar skull fracture suspected
 NO nasal intubation
 NO nasal gastric tubes
Basal Skull Fractures
CSF leaks
-rhinorrhea (nose)
-otorrhea (ear)
Tests for CSF:
Positve glucose
Positive Halo
Basal Skull Fracture
VIIth (Facial) Nerve Palsy
 Occur immediately
 Occur a few days after initial injury
Cerebral Contusion
 Cerebral contusions




fairly common
Mostly occur in frontal
and temporal lobes
Bruising of the brain
tissue without puncture
of pia
Petechial hemorrhages
Extravasation of fluid
from vessels
Cerebral Contusion
 Distinction between contusion and traumatic intracerebral
hematoma ill defined.
 Contusions, can evolve into an intracerebral hematoma
Cerebral Contusion
Blunt force
 High velocity
 Low velocity
Cerebral Contusion
 Intervention
 Decrease ICP
 Mannitol to decrease water content in brain
 Increase venous outflow
 Discuss with family/patient evolution of contusion
and need for monitoring
 Discuss bizarre behavior- frontal lobe
 Assist family in understanding a contusion to brain
stem has injured “awake” center in brain
Epidural Hematoma
 Located outside the
dura, within the skull
 Biconvex or lenticular
in shape
 Mostly located in
temporal or
temporoparietal region
Epidural Hematoma
 Result from tearing of
middle meningeal
artery D/T fracture
 Bleeds arterial in origin
 Does not tamponade
 50% mortality
Epidural Hematoma
 Brief loss of
consciousness followed
by “lucid interval” then
rapidly progressive
deterioration
 “Talk and die”
Epidural Hematoma
 Bleeding can rapidly
become mass lesion
 Cause
 IICP
 Brain shift
 Uncal herniation
Subdural Hematoma
 More common than
epidural hematomas
 30% of severe head
injuries
 Tearing of bridging
vein between cerebral
cortex and a draining
venous sinus
Subdural Hematoma
 Cover entire surface of
hemisphere
Subdural Hematoma
 Presentation can be
 Acute < 48 hours
 Subacute 2 days to 3
weeks
 More frequent in
elderly
 Chronic > 3 weeks
Subdural Hematoma
 Clinical findings range
from headache with
nausea to comatose and
flaccid
Subdural Hematoma
 Non-contrast CT scan
 Crescent shaped mass
 Ancillary tests
 CBC
 Chemistry
 Coag studies
 T&C
Subdural Hematoma
 Interventions
 Acute
Decrease ICP
 Nonacute
 Burr holes

Subarachnoid
Hemorrhage/Aneurysm rupture
 “worst h/a of my life”
 Aneurysms result from
thinning vascular wall
 Precipitated by
hypertensive event
 Straining
 Sex
 Heavy lifting
Subarachnoid
Hemorrhage/Aneurysm rupture
After rupture vessel
clamps down to
prevent further
bleeding
 Result in
 Ischemia/infarction
 Blood in subarachnoid
space is irritant
 Meningeal signs
Subarachnoid
Hemorrhage/Aneurysm rupture
Complications
 Increased ICP
 Vasospasm
 Rebleeding
 Ischemia
 Infarction
 Hydrocephalus
Subarachnoid
Hemorrhage/Aneurysm rupture
 Interventions
 ABC’s
 Monitor neuro status
 Fluids within normal range avoid dehydration
increases hemoconcentration, increases vasospasm
 Monitor sodium usually falls
 Normotensive BP until clipped then can be elevated
A foreign object
penetrates into
the skull and
brain
Penetrating/
Perforating Injuries
Perforating & Penetrating Trauma
Perforating
Penetrating
Hypoxia
Causes of
Secondary
Injury
Hypotension
Causes of
Secondary
Injury
Cerebral edema
1.Cerebrum
2. Skull
3. Cerebellum
4. Herniation of Brain Into
Spinal Column
Causes of Secondary Injury
Causes of
Secondary
Injury
Sustained hypertension
Causes of
Secondary
Injury
Hypercapnia
Seizures
Causes of
Secondary
Injury
Vasospasm
Causes of
Secondary
Injury
Causes of
Secondary
Injury
 Metabolic abnormalities (hypoglycemia)
 Ischemia (#1 cause)
Causes of Secondary Injury
Normal
Ischemic
MAP & ICP GO HAND IN HAND
MAP=
Diastolic
x2
Plus
Systolic
Divide
that by 3
ICP=
The
Brain
The
CSF
The
Blood
Cerebral Perfusion Pressure (CPP)
 Pressure required to maintain adequate
perfusion to cerebral tissues
 MAP – ICP = CPP
 Normal: 70-100 mmHg
CPP < 50 mmHg
 Results in Ischemia
Spinal Cord Injuries
 Involve bruising or
tearing of spinal cord
substance from
penetrating trauma or
a fracture/dislocation
of spinal column
 15-35 year olds
 Usually due to trauma
Spinal Cord Injuries
 Mechanism of Injury
 Axial loading
 Hyperflexion
 Hyperextension
 Injury may involve only
 Spinal cord
 Vertebral body
 Both
Spinal Cord Injuries
 Damage to cord
 From extrinsic(bony
and soft tissue injury)
 From intrinsic
(hemorrhage, edema,
hypoxia, biochemical
changes
Spinal Cord Injuries
Classification
 Complete
 Transection of the
cord, no preservation
of motor or sensory
function
 Incomplete
 Some cord sparing
Spinal Cord Injuries
Respiratory Complications
 Phrenic nerve innervates diaphragm, exits cervical cord at C-3, C-4, C-5
 if involved diaphragm involved
 Compromises ability to breath
 Intercostal muscles (T-1 to T-12) involved becomes difficult to deep
breath, cough
Neurogenic Shock
 Eliminates the “fight or
flight” protective
response and permits
the parasympathetic
system to function
unopposed
 Results in vasodilation
below level of the
injury, pooling of blood,
decreased venous return
to the heart, and
decreased cardiac
output
Neurogenic Shock
 Loss of ability to sweat
 Below level of injury
 D/T lack of innervation of sweat glands
 Temperature lower than normal
 D/T break in connection between hypothalamus and sympathetic
nervous system
 Loss of body heat by passively dilated vascular bed of skin
Neurogenic Shock
 Blood pressure may not be
restored by fluids alone
 In trying to normalize BP
may cause fluid overload,
pulmonary edema
 BP best restored by
judicious use of
vasopressors
 May perfuse adequately
without normal BP
Intravenous Fluids
Quadriplegic patients-may fail to become tachycardic or may
even become bradycardic in the presence of shock- due to
loss of cardiac sympathetic tone.
Intravenous Fluids
 Hypovolemic Shock
 Patient usually presents
with tachycardia
 Neurogenic Shock
 Patient usually presents
with bradycardia
If blood pressure does not improve after fluid challenge,
judicious use of vasopressors, may be indicated
Overzealous fluids may cause
PULMONARY EDEMA
in
Spinal Cord Injury Patients
Neurogenic
Shock
Orthostatic Hypotension
 Rapid drop in BP when vertical position assumed.
 Blood supply to brain inadequate, syncope results.
(brain damage and death can result)
 D/T loss of arteriole vasomotor tone below level of
lesion so there is pooling of blood in abdomen and
LE’s when upright.
 Seen in patients with lesions above T-7
Spinal Cord Injuries
Interventions
 ABC’s
 Cervical Spine
Immobilization
 O2
 Monitor VS, CO2
 Mechanical ventilation if
needed
 Monitor LOC, UOP
 Enhance venous return to
the heart
Interventions
 Support BP if needed
 Atropine if needed
 Methylprednisolone
 NG tube
 Foley
 Attempt to have someone
with patient most of the
time
Autonomic Hyperreflexia
 Noxious stimuli produces sympathetic discharge that
causes reflex vasoconstriction of blood vessels in skin
and visceral bed below level of the injury
 Vasoconstriction of visceral bed distends
baroreceptors in the carotid sinus and aortic arch,
body attempts to lower hypertension by superficial
dilation of vessels above level of injury
Autonomic Hyperreflexia
 As spinal shock reverses, potential for dysreflexia should
be considered in patients with injuries T-6 or above
 Nursing intervention – prevent conditions that are know
to trigger autonomic hyperreflexia
 Causative noxious stimulus most common
◦ Distended bladder d/t kinked drainage tube
Autonomic Hyperreflexia
Clinically
 Sudden hypertension 240/120
 Pounding headache
 Anxious
 Flushed face, neck, upper chest moistened with
perspiration
 Blurred vision
 Nasal congestion
 Nausea
 Lower extremities goose flesh, cold
Autonomic Hyperreflexia
Interventions
 Elevate HOB
 Relieve trigger mechanism
 Treat hypertension as needed
 Resources for family/patient for self care
Headaches
 Occur when there is traction, pressure, displacement,
inflammation or dilation of pain receptors in brain or
surrounding tissues
 Two types:
◦ Primary
 No organic cause consistently identified (migraines,
cluster, tension)
◦ Secondary
 Organic etiology (tumor, aneurysm, meningitis,
temporal arteritis)
Headaches
 Affects up to 75% population per year
 5% will seek treatment
 50 % of people with headache suffer migraine
 Mechanism unknown
 Blood vessels that supply brain and surrounding tissue
narrow, reduced blood flow, followed by reflex
vasodilatation, swelling, and inflammation of cerebral
blood vessels
Headaches
Assessment
 Hx of present illness
 Time frame
 onset (migraines early morning)
 Occurrence (in groups, then period of remission)
 Aura (migraines with/without aura)
 Duration (tension 7 days, migraine 4-72 hours)
Headaches
 Pain
 Character and quality
 Intensity
 Therapeutic measures implemented
 Success of therapeutic measures
 Location
 Unilateral (migraine), bilateral (tension), hatband
Headache
 Symptoms with migraines
 Aura possible
without aura most common
Nausea/vomiting
Photophobia
Difficulty concentrating
Visual changes
May see neurodeficits in “complicated” migraine






Headache
 Cluster Headaches
 Burning, sharp, severe unilateral orbital or temporal pain
 Photophobia
 Tearing, nasal congestion on affected side
 May have lid edema, red eye on affected side.
 Usually lasts < 1 hour, but may have multiple per day
Headaches
 Tension
 Dull, nonpulsating pain
 No photophobia, aura
 Usually starts at occiput and moves around bilaterally to
frontal area (band like)
Headaches
 Precipitating event
 Emotional (stress/depression)
 Metabolic (fever/menses)
 Flickering lights/television
 Alcohol abuse/withdrawal
 Food
 Fatigue or altered sleep wake cycle
Headaches
 Physical Exam
 Neuro exam
 Edema over the sinuses
 Distended, twitching scalp vessels
 Flushed, pale, or shiny skin
Headaches
 Diagnostic procedures (organic)
 Skull x-rays
 CT scan
Headaches
Interventions/Planning
 Physical measures
 Heat (muscular) or cold (vascular)
 Darkened room
 Massage
 Psychological measures
 Stress mgt
 Relaxation techniques
 Behavior modification
Headaches
Interventions
 Pharmacological measures
 Preventive drugs
 Vasoconstrictor agents
 Beta blockers
 Anticonvulsants
 Analgesics
 Oxygen
What Is Stroke ?
 A stroke occurs when
blood flow
to the brain is
interrupted by
a blocked or burst
blood vessel.
What Is the Impact of Stroke?
 Stroke is the third leading cause
of death in the United States
 On average, someone suffers
a stroke every 53 seconds
 About 600,000 Americans
suffer strokes each year
 Every 3.3 minutes, someone
dies of a stroke
What Is the Impact of Stroke?
 Stroke is a leading cause of
serious, long-term disability
 About 4 million Americans
are stroke survivors
 Stroke costs the U.S. $30
to $40 billion a year
Stroke
 Clinical syndrome consisting of a neurological deficit
resulting from an interuption of blood flow to an area of
the brain, rapid or gradual in onset, which persists for more
than 24 hours.
 Two types
 Ischemic: Thrombotic or embolic occlusion of a
cerebral artery resulting in infarction
 Hemorrhagic: Spontaneous rupture of a vessel resulting
in intracerebral or subarachnoid hemorrhage
Stroke
Assessment
 Hx present illness (time pattern)
 Classifications of stroke:
 TIA – brief, lasting seconds to hours; < 24 hrs
 RIND – lasting 48 hours or less, complete resolution of
deficit, reversible ischemic neuro deficit
 Stroke in evolution/progressive – Symptoms last >24
hrs with progressive neurologic deterioration.
 Completed stroke – permanent neurologic damage
Stroke
 Medical History
 Diabetes
 Rheumatic heart disease
 Recent MI
 CHF
 Migraines
 Hypertension
 A-Fib
Stroke
Physical Exam
 Anterior Circulation
 Alteration in LOC
 Motor deficit
 Contralateral
hemiparesis,
hemiplegia
 Sensory deficit
 Contralateral
Stroke
Physical Exam
 Anterior Circulation
 Speech deficit
 Dysphasia
 Expressive or receptive
 Dominant
hemisphere
 Visual deficit
 Loss of vision in half of
the visual field on same
side
Stroke
Physical Exam
 Posterior Circulation
(vertebral basilar)
 Alteration in LOC
 Motor deficit
 more than one limb
Stroke
Physical Exam
 Cranial nerve deficit
 Dysphonia
 difficulty producing voice
sounds
 Dysarthria
 difficulty in articulation
 Dysphagia
 difficulty in swallowing
Stroke
Physical Exam
 Posterior Circulation
(vertebral basilar)
 Visual deficits
 field defects,
 cortical blindness
 diplopia
 Loss of coordination
 Ataxia
Stroke
 Ischemic
 Sudden, rapid onset
 Occurs at sleep, rest
 Hemorrhagic
 Severe headache
 More gradual onset
 Symptoms of
increasing ICP
 Occurs during
activity
Stroke
 Interventions
 Maintain airway, breathing, circulation
 Monitor neuro status for change
 Maintain venous outflow (head neutral position)
 Frequently monitor



Cerebral function
LOC
Blood pressure
Stroke
 Interventions
 Supplemental oxygen, pulse oximetry
 RSI: sedation, neuromuscular blockers, analgesics
 Initiate measures to normalize blood pressure
 Keep SBP < 180, DBP <105
 Labetalol drug of choice.
 Avoid rapid BP decreases. Want BP high enough to perfuse.
 Administer anticoagulation therapy (ischemic stroke in
evolution only)
 May use meds to cause coagulation in hemorrhagic stroke


FFP
Vitamin K
Stroke
 Interventions
 Administer IV
thrombolytics
(ischemic stroke)

Patient must
present within 3
hours of onset of
symptoms, CT
must exclude
intracranial
hemorrhage
Stroke
Interventions:
 Surgical interventions
 Carotid endarterectomy
( TIAs)
 Intra-arterial
fibrinolytic therapy (6
hr limit)
 Angioplasty/stent
placement
Communicating
• An overproduction (Pediatric
Tumors)
• Under reabsorption of CSF
(Subarachnoid Hemorrhages)
Non Communicating
• A blockage or destruction
of the channels of CSF
Drainage
• Causes include Tumors,
Encephalitis, Spina Bifida)
Shunt Problems
 Shunt purpose- relieve increased ICP from
hydrocephalus
 Diversion relieves obstruction by creating
alternative pathways for free circulation and/or
absorption of CSF
 Most common complications
 Infections
 Shunt malfunction
 D/T obstruction(plugging by blood clots, brain or
malfunction
 Assessment
Shunt Problems
 Hx of present illness
Type of shunt
 Length of
implantation
 Medical history
 Reason for shunt
 Previous problems
with shunt
 Risk factors- growth

 Physical Exam
 Shunt malfunction

Mental status:




Shunt
Problems
Decreased alertness
Decreased intellectual function
Behavioral changes
Eye changes


Inability to look up
Alteration in visual acuity or fields
Shunt Problems
 Shunt Malfunction
 Incontinence
 Gait/coordination
changes
 Vomiting
 Infant:
 Tense fontanelles
 Shrill cry
 Loss of appetite
 Physical Exam
Shunt
Problems
 Infection
 Fever
 Meningeal signs
 Altered Mental status
 Diagnostic procedures
 CT scan
 Lumbar puncture for CSF analysis
Shunt
 Monitor vital signs
Problems
 Prepare and assist for lumbar puncture/shunt tap
 Interventions
 CSF for analysis/culture
 Antibiotic therapy
Seizures
 Sudden, paroxysmal discharge of a group of neurons
resulting in transient impairment of consciousness,
movement, sensation, or memory
 Trigger causes abnormal burst of electrical stimulus,
disrupts brain’s normal nerve conduction
 Causes
 Ionic
Electrolyte imbalance
 Metabolic
 Hyperglycemia
 Fever
 Stress
 Nerve cell structural changes
 Hypoxia, tumors, trauma

Seizures
Seizures
 Classification
 Generalized
 Involves all areas of
both cerebral
hemispheres
 Motor manifestations
are bilateral
 Classification
 Partial
 Focal onset involving
one particular part of
the brain
 Status Epilepticus
Seizures
 Medical emergency
 Series of seizures without recovery of baseline neuro
status between seizures
 Lead to mortality and morbidity from




Acidemia
Hypoglycemia
Autonomic dysfunction
Hypercalcemia
Seizures
 At Risk
 Head trauma, stroke, CNS infections,Degenerative CNS
disorders(MS)
Seizures
 Assessment
 Hx present illness






Precipitating event (fever)
Site of origin, spread of
seizure
Motor activity
Duration and frequency
LOC
Postictal behavior
Seizures
 Assessment
 Medical history






Seizure history
Congenital anomalies
Metabolic abnormalities
Neurological disease (tumors, infectious process)
Recent trauma
Pharmacological hx (excessive lax in kids)
Seizures
 Assessment
 Physical exam (during and after sz)
LOC
 Responsive to stimuli ( what kind of stimuli?)
 Ability to follow commands
 Motor activity (type and origin of spread)
 Tonic phase
 Contraction of voluntary muscles, body stiffens
 Clonic phase
 Violent, rhythmic contractions

Seizures
 Assessment
 Physical exam (during and after sz)




Eye deviation
Incontinence
Temperature
Postictal State
 LOC
 Weakness of one limb
 Headache, amnesia
 Duration
 Assessment
Seizures
 Physical exam (during and after sz)


Physical injury sustained
Recurrence of the seizure
 Assessment
Seizures
 Diagnostic procedures
Therapeutic monitoring of anticonvulsant drug levels (seizure
pts)
 No history
 CT scan, MRI
 EEG follow up appt
 Lumbar puncture
 CBC
 Lytes, glucose, BUN, Cr
 Toxicology screen

Seizures
 Interventions
 Maintain airway, breathing, circulation
 Turn pt to side, protect from injury
 Loosen tight or restrictive clothing
 Suction, if necessary
 Supplemental oxygen
 Establish IV access
 Pharmacological support to stop seizures


Diazepam IV
Lorazepam IV
 Interventions
Seizures
 Pharmacological support to prevent recurrence


Phenytoin, IV
Fosphenytoin IV or IM
 Interventions
 Monitor
Seizures
Neurological status
 Temperature, vital signs
 Pharmacological support to prevent or correct
complications
 50% glucose IV
 Thiamine IM or IV

Seizures
 Interventions
 Observation until
recovered from postictal
state
 Monitor neuro
recovery
 Seizure precautions
 Monitor therapeutic
drug levels
 Assess pt’s perceived
compliance
 Interventions
 Assess for
compliance
 Discharge Teaching


Medications
Consequences of
noncompliance
 Follow up appts.