Neurological Emergencies. Surgical Neurological Emergencies Increased Intracranial Pressure Concussion Skull Fractures Contusion Epidural Hematoma Subdural

Neurological EmergenciesNeurological Emergencies

Surgical Neurological Surgical Neurological EmergenciesEmergencies

Increased Intracranial Pressure

ConcussionSkull FracturesContusionEpidural HematomaSubdural hematoma

Subarachnoid Hemorrhage

Aneurysm RuptureSpinal Cord InjuriesAutonomic

Dysreflexia

Medical Medical Neurological EmergenciesNeurological Emergencies

HeadacheStroke

Shunt Problem

AssessmentAssessment


AssessmentAssessmentATLS- Primary Survey

◦A –Alert◦V – Responds to Vocal stimulus◦P – Responds to Painful stimulus◦U –Unresponsive to ALL stimulus

Glasgow Coma ScaleMotor Response Pupillary StatusVital Signs

AssessmentAssessment◦Awareness (ability to interact with and interpret

environment)

◦Orientation (person, place, time)

◦Memory (short and long)

◦Judgment and reasoning◦Communications (verbalization and comprehension)

Follow Commands

◦Attention span◦Knowledge of current events


Motor Strength

AssessmentAssessmentGLASGOW COMA SCALE

◦Best Eye Opening◦Best Verbal Response◦Best Motor Response


Best Eye Opening

Spontaneously……………..….4 To Verbal Command………….3 To Pain………………………….2 No Response…………………..1

AssessmentAssessmentBest Verbal Response

Oriented, Converses…………….5 Disoriented, Converses…………4 Inappropriate words………….….3 Incomprehensible sounds……….2 No Response…………………..…1

AssessmentAssessmentBest Motor Response

◦Obeys Commands……..….…………..6

◦To Pain Localizes Pain……………….…….5 Flexion Withdrawal…………….….4 Abnormal Flexion……………...….3 Abnormal Extension………………2 No Response……………………...1


Glasgow Coma Scale

PediatricsVerbal (2 to 5 years)

◦Appropriate words or phrases………..5

◦Inappropriate words…………………...4◦Persistent cries and/or screams…..…

3

AssessmentAssessmentGlasgow Coma Scale

PediatricsVerbal (0 to 23 months)

◦Smiles or coos appropriately…………5

◦Cries and consolable…………………4◦Persistent inappropriate crying

and / or screaming…………………..3


Mild◦ GCS Score 14-15

Moderate◦ GSC Score 9-13

Severe◦ GCS Score 3-8

Severity of InjurySeverity of Injury

A desk scores a “3”A desk scores a “3”


Size Shape

Spherical Symmetrical Beware of the oval pupil

CN III compression

Reaction Hippus – fails to hold constriction with light on

Pupillary ResponsePupillary Response

Etiologies of Altered LOCEtiologies of Altered LOC

Hyperarousability◦ Trauma◦ Shock◦ Hypoxia◦ Metabolic abnormalities◦ Alcohol◦ Medications or illicit drugs◦ Endocrine disturbances◦ Hyperthermia◦ Psychiatric illness

Hypoarousability◦ Trauma◦ Shock◦ Hypoxia◦ Metabolic

abnormalities◦ Alcohol◦ Medications or illicit

drugs◦ Endocrine

disturbances◦ Hyperthermia◦ Psychiatric illness

Loss of ConsciousnessLoss of Consciousness“A,E,I,O,U TIPS”“A,E,I,O,U TIPS”

A◦ Alcohol

E◦ Epilepsy

I◦ Insulin (too much, too

little)O

◦ Oxygen (too much, too little)

U◦ Uremia or other

metabolic issues

T◦ Trauma, toxicity, tumors,

thermoregulationI

◦ Infections, ischemiaP

◦ Psychiatric, poisoningsS

◦ 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)

PosturingPosturing

Abnormal posturing is a late sign of increasing ICP◦Decorticate

Abnormal flexion

◦Decerebrate Abnormal

extension

Meningeal SignsMeningeal SignsNuchal rigidity

◦Stiff neck, pain on flexionPhotophobiaPositive Brudzinski’s

◦Involuntary flexion of knees/hips when neck flexed

Positive Kernig’s◦Unable to straighten leg when hip fully

flexed in supine patient

Surgical Neurological Surgical Neurological EmergenciesEmergencies

Reviewing the brain…Reviewing the brain…

Our brains are just like Emergency Room Nurses………….

Our heads are hard!

The skull is hard!! It does not stretch or expand!

We are ALWAYS hungry!

◦The brain needs a constant supply of oxygen and glucose. It cannot store glucose OR oxygen

Don’t worry…..I just have time for a quick bite on the run!!!

We may be tough on the outside…..

……But we’re softies on the But we’re softies on the inside.inside.

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Increased Intracranial Increased Intracranial PressurePressureThe skull is a rigid

box and within that box are these components◦ Brain 80%◦ Blood 10%◦ CSF 10%

The volume of the intracranial components must remain constant

Cerebral CompensationCerebral Compensation

CSF◦ Shunting intracerebral

fluid to ventricles◦ Too slow in trauma

Brain ◦ Herniation◦ Not user friendly to pt

Blood◦ Vasoconstriction /

vasodilation

I’m really in trouble now!!!

Intracranial PressureIntracranial PressureIntracranial 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 Increased Intracranial PressurePressure

Initially -intracranial volume increases-ICP 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 Increased Intracranial PressurePressureAssessmentEarly 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


Early Increasing ICP Motor function

Usually contralateral to lesion Pronator drift Loss of one or more grades on the

strength scale Increased tone


Early Increasing ICP◦Pupils Sluggish to light response Usually unilateral Ipsilateral to lesion Papilledema or bulging of optic discs

Blurred vision


Early Increasing ICP◦Vital signs Occasionally tachycardic Occasional hypertensive swings

Increased Intracranial Increased Intracranial PressurePressureLate Increasing ICP

◦LOC Arousable only with deep pain Unarousable

◦Motor function Dense hemiparesis Abnormal flexion Abnormal extension No response (flaccidity preliminary to

death)

PosturingPosturing

Abnormal posturing is a late sign of increasing ICP◦Decorticate

Abnormal flexion

◦Decerebrate Abnormal

extension


Decreased LOC Motor Dysfunctions Pupillary abnormalities Impaired Reflexes Changes in Vital Signs Irregular respirations

Sign & Symptoms-Impending Herniation


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 PressureIncreased Intracranial PressureHerniationHerniation

Increased Intracranial Increased Intracranial PressurePressureInterventionsABC’sMechanically decrease ICPHyperventilationOsmotic Agents


Lowering CO2 controversialless than 30 mmHg, may cause

hypoperfusion, and can be correlated to decreasing survival rates(decreases CBF)

May be needed for Brief periods- acute neurological deterioration or longer in some specific cases.

Vasoconstricts vessels and reduces CBFAggressive hyperventilation may cause

cerebral ischemia

HyperventilationHyperventilationGoal is to keep CO2 low range of normalGoal is to keep CO2 low range of normal


Osmotic Agents

Mannitol:◦IV push◦reduces ICP within 15 minutes with

continued effectiveness for 2-3 hours◦max dose 1gm/kg q 3 hours◦Monitor serum osmolarity

Increased Intracranial Increased Intracranial PressurePressureTreatment of ICP

◦ Easiest to manipulate is BP and CSF

◦ proper head alignment

◦ sedation◦ Surgery

Goal◦Keep SBP>90

ConcussionConcussionTransient 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

ConcussionConcussion

Traumatic reversible neurological deficit

Reversible in minutes to hours

Retrograde or antegrade amnesia

ConcussionConcussion

Diagnosis◦CT scan

Rule out other injury

◦Clinical picture◦History of injury

ConcussionConcussionInterventions

◦Assess neuro status◦Patient/Family education return to

facility Change in LOC Change in pupils Projectile vomiting Seizure Inability to arouse


◦Educate patient/family Post concussion syndrome

H/A Dizziness (positional) Tinnitus Inability to concentrate Personality change Memory disturbances


◦Educate patient/family Post concussion syndrome

Duration Days to years

Social/occupational Difficulty school/work

Skull FracturesSkull Fractures

Fractures Cranial vault◦ Skull base◦ Linear◦ Open◦ Closed

Basal Skull Fractures

Periorbital ecchymosis

(Raccoon sign)

Anterior fracture

Basal Skull fractureBasal Skull fracture

Retroauricular ecchymosis

(Battle’s sign)--Posterior fracture

Blood behind tympanic membrane

--Middle Fracture

Basilar Fractures cont’dBasilar Fractures cont’dIf 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

Skull Fractures

Fragments depressed more than the thickness of the skull require surgical elevation

Open or compound skull fractures

Dura often tornRequires early

surgical repair


ComplicationsInfectionsHematomaCSF leaksLoss of smellLoss of hearingSeizurespneumocephalus


Interventions◦ABC’s◦Monitor for

seizures◦Monitor for CSF

leak◦Avoid nasal

intubation, nasal gastric tube, nose blowing, sneezing

◦Interventions Anticonvulsants

as ordered Antibiotics as

ordered Possible surgery

Cerebral ContusionCerebral ContusionCerebral contusions fairly

commonMostly occur in frontal and

temporal lobesBruising of the brain tissue

without puncture of pia Petechial hemorrhagesExtravasation of fluid from

vessels

Cerebral ContusionCerebral ContusionDistinction between contusion

and traumatic intracerebral hematoma ill defined.

Contusions, can evolve into an intracerebral hematoma

Cerebral ContusionCerebral Contusion

Blunt force High velocity Low velocity

Cerebral ContusionCerebral Contusion

Coup - contracoupCoup - contracoup injuryinjury

Cerebral ContusionCerebral ContusionIntervention

◦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 HematomaEpidural 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 tamponade50% mortality


Brief loss of consciousness followed by “lucid interval” then rapidly progressive deterioration

“Talk and die”


Bleeding can rapidly become mass lesion

Cause ◦ IICP◦ Brain shift◦ Uncal herniation



Interventions◦ ABC’s◦ GCS <8

Intubate

◦ Decrease ICP◦ Monitor neuro status◦ SURGERY for clot

evacuation

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 HematomaSubdural 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

massAncillary tests

◦CBC◦Chemistry◦Coag studies◦T&C

Subdural HematomaSubdural Hematoma

Interventions◦Acute Decrease ICP

◦Nonacute Burr holes

Subarachnoid Subarachnoid Hemorrhage/Aneurysm ruptureHemorrhage/Aneurysm rupture“worst h/a of my

life”Aneurysms result

from thinning vascular wall

Precipitated by hypertensive event◦ Straining◦ Sex◦ Heavy lifting

Subarachnoid Subarachnoid Hemorrhage/Aneurysm ruptureHemorrhage/Aneurysm ruptureAfter rupture vessel

clamps down to prevent further bleeding

Result in◦ Ischemia/infarction

Blood in subarachnoid space is irritant◦ Meningeal signs

Subarachnoid Subarachnoid Hemorrhage/Aneurysm ruptureHemorrhage/Aneurysm ruptureComplicationsIncreased ICPVasospasmRebleedingIschemiaInfarctionHydrocephalus

Subarachnoid Subarachnoid Hemorrhage/Aneurysm Hemorrhage/Aneurysm ruptureruptureInterventions

◦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

Spinal Cord InjuriesSpinal Cord Injuries

Involve bruising or tearing of spinal cord substance from penetrating trauma or a fracture/dislocation of spinal column

15-35 year oldsUsually due to

trauma


Mechanism of Injury◦ Axial loading◦ Hyperflexion◦ Hyperextension

Injury may involve only◦ Spinal cord◦ Vertebral body◦ Both


Damage to cord◦ From extrinsic(bony

and soft tissue injury)

◦ From intrinsic (hemorrhage, edema, hypoxia, biochemical changes


Classification ◦Complete

Transection of the cord, no preservation of motor or sensory function

◦Incomplete Some cord sparing


Respiratory ComplicationsPhrenic nerve innervates

diaphragm, exits cervical cord at C-3, C-4, C-5 ◦if involved diaphragm involved

Compromises ability to breathIntercostal muscles (T-1 to T-12)

involved becomes difficult to deep breath, cough

Neurogenic ShockEliminates 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 ShockLoss of ability to sweat

◦Below level of injury◦D/T lack of innervation of sweat

glandsTemperature 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 FluidsQuadriplegic

patients-may fail to become

tachycardic or may even become bradycardic in the

presence of shock- due to loss

of cardiac sympathetic tone.

Intravenous FluidsIntravenous Fluids

Hypovolemic Shock Patient usually presents

with tachycardia

Neurogenic Shock Patient usually presents

with bradycardia

Overzealous fluids may cause PULMONARY EDEMA

in Spinal Cord Injury Patients

If blood pressure does not improve after fluid challenge, judicious use of vasopressors, may be indicated

Neurogenic ShockOrthostatic HypotensionRapid 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


InterventionsABC’sCervical Spine

ImmobilizationO2Monitor VS, CO2Mechanical ventilation

if neededMonitor LOC, UOPEnhance venous

return to the heart

InterventionsSupport BP if

neededAtropine if neededMethylprednisoloneNG tubeFoleyAttempt to have

someone with patient most of the time

Autonomic HyperreflexiaNoxious 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 HyperreflexiaAs 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

ClinicallySudden hypertension 240/120Pounding headacheAnxious Flushed face, neck, upper chest moistened

with perspirationBlurred visionNasal congestionNauseaLower extremities goose flesh, cold

Autonomic HyperreflexiaInterventions

◦Elevate HOB◦Relieve trigger mechanism◦Treat hypertension as needed◦Resources for family/patient for self

care

Medical Medical Neurological EmergenciesNeurological Emergencies

HeadachesHeadachesOccur 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)

HeadachesHeadachesAffects up to 75% population per year5% will seek treatment50 % of people with headache suffer

migraineMechanism unknown

◦Blood vessels that supply brain and surrounding tissue narrow, reduced blood flow, followed by reflex vasodilatation, swelling, and inflammation of cerebral blood vessels

HeadachesHeadachesAssessmentHx 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)

HeadachesHeadachesPain

◦Character and quality◦Intensity◦Therapeutic measures implemented◦Success of therapeutic measures

Location◦Unilateral (migraine), bilateral

(tension), hatband

HeadacheHeadacheSymptoms with migraines

◦Aura possible without aura most common

◦Nausea/vomiting◦Photophobia◦Difficulty concentrating◦Visual changes◦May see neurodeficits in

“complicated” migraine

HeadacheHeadacheCluster 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

HeadachesHeadachesTensionDull, nonpulsating painNo photophobia, auraUsually starts at occiput and

moves around bilaterally to frontal area (band like)

HeadachesHeadachesPrecipitating event

◦Emotional (stress/depression)◦Metabolic (fever/menses)◦Flickering lights/television◦Alcohol abuse/withdrawal◦Food◦Fatigue or altered sleep wake cycle

HeadachesHeadaches

Physical Exam◦Neuro exam◦Edema over the sinuses◦Distended, twitching scalp vessels◦Flushed, pale, or shiny skin

HeadachesHeadachesDiagnostic procedures (organic)

◦Skull x-rays◦CT scan

HeadachesHeadachesInterventions/PlanningPhysical measures

◦ Heat (muscular) or cold (vascular)◦ Darkened room◦ Massage

Psychological measures◦ Stress mgt◦ Relaxation techniques◦ Behavior modification

HeadachesHeadaches

InterventionsPharmacological measures

◦Preventive drugs Vasoconstrictor agents Beta blockers Anticonvulsants

◦Analgesics◦Oxygen

HeadachesHeadaches

InterventionsInstructions regarding

medicationsPurposeTimingSide effects

StrokeStrokeClinical 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

StrokeStrokeClinical picture depends on vessel

involved, extent of damage, and collateral flow

500,000 new cases per yearMost common in 65 years and older45 % are womenHigh Risk

◦TIA’s or previous stroke◦CHF, mitral valve disorders, a-fib, diabetes,

HTN

StrokeStrokeAssessmentHx 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

StrokeStrokeMedical History

◦Diabetes◦Rheumatic heart disease◦Recent MI◦CHF◦Migraines◦Hypertension◦A-Fib

StrokeStroke

Physical ExamAnterior Circulation

◦Alteration in LOC◦Motor deficit

Contralateral hemiparesis, hemiplegia

◦Sensory deficit Contralateral

StrokeStroke

Physical ExamAnterior Circulation

◦Speech deficit Dysphasia Expressive or

receptive Dominant hemisphere

◦Visual deficit Loss of vision in half

of the visual field on same side

StrokeStroke

Physical ExamPosterior Circulation

(vertebral basilar)◦Alteration in LOC◦Motor deficit

more than one limb

StrokeStrokePhysical ExamCranial nerve deficit

◦Dysphonia difficulty producing

voice sounds◦Dysarthria

difficulty in articulation

◦Dysphagia difficulty in

swallowing

StrokeStrokePhysical ExamPosterior

Circulation (vertebral basilar)◦Visual deficits

field defects, cortical blindness diplopia

◦Loss of coordination

◦Ataxia

StrokeStroke

Ischemic◦ Sudden, rapid

onset◦ Occurs at sleep,

rest

Hemorrhagic◦ Severe headache◦ More gradual

onset◦ Symptoms of

increasing ICP◦ Occurs during

activity

StrokeStrokeDiagnostic Procedures

◦STAT CT scan◦MRI

StrokeStrokeInterventions

◦Maintain airway, breathing, circulation

◦Monitor neuro status for change◦Maintain venous outflow (head

neutral position)◦Frequently monitor

Cerebral function LOC Blood pressure


◦ 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


◦Administer IV thrombolytics (ischemic stroke) Patient must present within 3 hours

of onset of symptoms, CT must exclude intracranial hemorrhage

StrokeStroke

Interventions:Surgical

interventions◦ Carotid

endarterectomy ( TIAs)

◦ Intra-arterial fibrinolytic therapy (6 hr limit)

◦ Angioplasty/stent placement

Shunt ProblemsShunt ProblemsShunt purpose- relieve increased ICP

from hydrocephalusDiversion 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

Shunt ProblemsShunt ProblemsAssessment

◦Hx of present illness Type of shunt Length of

implantation◦Medical history

Reason for shunt Previous problems

with shunt◦Risk factors-

growth

Shunt ProblemsShunt ProblemsPhysical Exam

◦Shunt malfunction Mental status:

Decreased alertness Decreased intellectual function Behavioral changes

Eye changes Inability to look up Alteration in visual acuity or fields

Shunt ProblemsShunt Problems

Shunt Malfunction◦Incontinence◦Gait/coordination

changes◦Vomiting◦Infant:

Tense fontanelles Shrill cry Loss of appetite

Shunt ProblemsShunt ProblemsPhysical Exam

◦Infection Fever Meningeal signs Altered Mental status

◦Diagnostic procedures CT scan Lumbar puncture for CSF analysis

Shunt ProblemsShunt ProblemsInterventions

◦Monitor vital signs◦Prepare and assist for lumbar

puncture/shunt tap◦CSF for analysis/culture◦Antibiotic therapy

SeizuresSeizuresSudden, 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

SeizuresSeizuresCauses

◦Ionic Electrolyte imbalance

◦Metabolic Hyperglycemia Fever Stress

◦Nerve cell structural changes Hypoxia, tumors, trauma

SeizuresSeizures

Classification◦Generalized

Involves all areas of both cerebral hemispheres

Motor manifestations are bilateral

Classification◦Partial

Focal onset involving one particular part of the brain

SeizuresSeizuresStatus Epilepticus

◦Medical emergency◦Series of seizures without recovery

of baseline neuro status between seizures

◦Lead to mortality and morbidity from Acidemia Hypoglycemia Autonomic dysfunction Hypercalcemia

SeizuresSeizures

At Risk◦Head trauma, stroke, CNS

infections,Degenerative CNS disorders(MS)

SeizuresSeizures

Assessment ◦Hx present illness

Precipitating event (fever)

Site of origin, spread of seizure

Motor activity Duration and

frequency LOC Postictal behavior

SeizuresSeizuresAssessment

◦Medical history Seizure history Congenital anomalies Metabolic abnormalities Neurological disease (tumors, infectious

process) Recent trauma Pharmacological hx (excessive lax in

kids)


◦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


◦Physical exam (during and after sz) Eye deviation Incontinence Temperature Postictal State

LOC Weakness of one limb Headache, amnesia Duration


◦Physical exam (during and after sz) Physical injury sustained Recurrence of the seizure


◦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

SeizuresSeizuresInterventions

◦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


◦Pharmacological support to prevent recurrence Phenytoin, IV Fosphenytoin IV or IM


◦Monitor Neurological status Temperature, vital signs

◦Pharmacological support to prevent or correct complications 50% glucose IV Thiamine IM or IV

SeizuresSeizures

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.

Documents

Neurological Emergencies. Surgical Neurological Emergencies Increased Intracranial Pressure Concussion Skull Fractures Contusion Epidural Hematoma Subdural