Neurological Emergencies

Neurological Emergencies

Surgical Neurological Emergencies
Increased Intracranial Pressure Concussion Skull Fractures Contusion Epidural Hematoma Subdural hematoma Subarachnoid Hemorrhage Aneurysm Rupture Spinal Cord Injuries Autonomic Dysreflexia

Medical Neurological Emergencies
Headache Stroke Shunt Problem

Assessment

Assessment A - airway B - breathing C - circulation D - DISABILITY

Assessment ATLS- Primary Survey Glasgow Coma Scale Motor Response
A –Alert V – Responds to Vocal stimulus P – Responds to Painful stimulus U –Unresponsive to ALL stimulus Glasgow Coma Scale Motor Response Pupillary Status Vital Signs

Assessment 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

Assessment Motor Strength

Assessment 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

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

Assessment Best Motor Response Obeys Commands……..….…………..6 To Pain
Localizes Pain……………….…….5 Flexion Withdrawal…………….….4 Abnormal Flexion……………...….3 Abnormal Extension………………2 No Response……………………...1

Assessment Glasgow Coma Scale Pediatrics Verbal (2 to 5 years)
Appropriate words or phrases………..5 Inappropriate words…………………...4 Persistent cries and/or screams…..…3

Assessment 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 Assessment Mild Moderate Severe GCS Score 14-15
GSC Score 9-13 Severe GCS Score 3-8

A desk scores a “3”

Assessment Pupillary Response Size Shape Reaction
Spherical Symmetrical Beware of the oval pupil CN III compression Reaction Hippus – fails to hold constriction with light on

Etiologies of Altered LOC
Hypoarousability Trauma Shock Hypoxia Metabolic abnormalities Alcohol Medications or illicit drugs Endocrine disturbances Hyperthermia Psychiatric illness Hyperarousability Trauma Shock Hypoxia Metabolic abnormalities Alcohol Medications or illicit drugs Endocrine disturbances Hyperthermia Psychiatric illness

Loss of Consciousness “A,E,I,O,U TIPS”
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, thermoregulation I Infections, ischemia P Psychiatric, poisonings S Stroke, syncope or other neurologic / cardiovascular causes

Assessment 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)

Posturing Abnormal posturing is a late sign of increasing ICP
Decorticate Abnormal flexion Decerebrate Abnormal extension

Meningeal Signs Nuchal rigidity Photophobia Positive Brudzinski’s
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

Surgical Neurological Emergencies

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 inside.

Increased Intracranial Pressure
Neurological Emergencies July 30, 2004 Increased Intracranial Pressure The 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 Monro-Kellie Doctrine As one component increases the other two will decrease in an attempt to compensate and thus keep ICP within normal limits, despite increasing pathology. Because of this the brain will demonstrate only slight increases in pressure over a wide range of expansion in volume. As pathology progresses, the compensatory mechanisms are depleted, which results in a rapid increase in ICP with ONLY small increase in volume. THIS produces a shift of the brain contents, with herniation of the brain through the tentorial opening, resultant pressure on the brain stem, clinical picture of altered level of consciousness as well as pupillary, motor, and vital sign changes CEN Review Course

Cerebral 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 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

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

Neurological Emergencies July 30, 2004 Increased Intracranial Pressure Compensatory mechanisms are depleted. Results in rapid increase in ICP with only a small increase in volume. Produces a shift of brain contents to area of lesser pressure, herniation then occurs. CEN Review Course

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

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

Late Increasing ICP LOC Arousable only with deep pain Unarousable Motor function Dense hemiparesis Abnormal flexion Abnormal extension No response (flaccidity preliminary to death)

Posturing Abnormal posturing is a late sign of increasing ICP
Decorticate Abnormal flexion Decerebrate Abnormal extension

Sign & Symptoms- Impending Herniation Decreased LOC Motor Dysfunctions Pupillary abnormalities Impaired Reflexes Changes in Vital Signs Irregular respirations

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 Herniation
Neurological Emergencies July 30, 2004 Increased Intracranial Pressure Herniation As ICP rises, CPP decreases, leading to cerebral ischemia and potential for hypoxia, with secondary insult CEN Review Course

Interventions ABC’s Mechanically decrease ICP Hyperventilation Osmotic Agents

Hyperventilation Goal is to keep CO2 low range of normal Lowering CO2 controversial less 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 CBF Aggressive hyperventilation may cause cerebral ischemia

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

Treatment of ICP Easiest to manipulate is BP and CSF proper head alignment sedation Surgery

Goal Keep SBP>90

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 Traumatic reversible neurological deficit
Reversible in minutes to hours Retrograde or antegrade amnesia

Concussion Diagnosis CT scan Clinical picture History of injury
Rule out other injury Clinical picture History of injury

Concussion Interventions Assess neuro status
Patient/Family education return to facility Change in LOC Change in pupils Projectile vomiting Seizure Inability to arouse

Concussion Interventions Educate patient/family
Post concussion syndrome H/A Dizziness (positional) Tinnitus Inability to concentrate Personality change Memory disturbances

Concussion Interventions Educate patient/family
Post concussion syndrome Duration Days to years Social/occupational Difficulty school/work

Skull Fractures Fractures Cranial vault Skull base Linear Open Closed

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

Skull Fractures Fragments depressed more than the thickness of the skull require surgical elevation Open or compound skull fractures Dura often torn Requires early surgical repair

Skull Fractures Complications Infections Hematoma CSF leaks
Loss of smell Loss of hearing Seizures pneumocephalus

Skull Fractures Interventions 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 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

Coup - contracoup injury
Cerebral Contusion Coup - contracoup injury

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

Epidural Hematoma

Epidural Hematoma Interventions ABC’s GCS <8 Decrease ICP
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 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 Ancillary tests
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

After rupture vessel clamps down to prevent further bleeding Result in Ischemia/infarction Blood in subarachnoid space is irritant Meningeal signs

Complications Increased ICP Vasospasm Rebleeding Ischemia Infarction Hydrocephalus

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

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 Injury may involve only
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 Incomplete
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 Neurogenic 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 Support BP if needed
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
Neurological Emergencies July 30, 2004 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 CEN Review Course

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

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

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

Medical Neurological Emergencies

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 Location Character and quality Intensity
Therapeutic measures implemented Success of therapeutic measures Location Unilateral (migraine), bilateral (tension), hatband

Headache Symptoms with migraines Aura possible Nausea/vomiting
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

Headaches Interventions Instructions regarding medications Purpose
Timing Side effects

Neurological Emergencies
July 30, 2004 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 CEN Review Course

Stroke Clinical picture depends on vessel involved, extent of damage, and collateral flow 500,000 new cases per year Most common in 65 years and older 45 % are women High Risk TIA’s or previous stroke CHF, mitral valve disorders, a-fib, diabetes, HTN

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 Dysarthria
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 Hemorrhagic Severe headache Sudden, rapid onset
Occurs at sleep, rest Hemorrhagic Severe headache More gradual onset Symptoms of increasing ICP Occurs during activity

Stroke Diagnostic Procedures STAT CT scan MRI

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

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

Shunt Problems Assessment Hx of present illness Medical history
Type of shunt Length of implantation Medical history Reason for shunt Previous problems with shunt Risk factors- growth

Shunt Problems Physical 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 Problems Shunt Malfunction Incontinence
Gait/coordination changes Vomiting Infant: Tense fontanelles Shrill cry Loss of appetite

Shunt Problems Physical Exam Infection Diagnostic procedures Fever
Meningeal signs Altered Mental status Diagnostic procedures CT scan Lumbar puncture for CSF analysis

Shunt Problems Interventions Monitor vital signs
Prepare and assist for lumbar puncture/shunt tap 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

Seizures Causes Ionic Metabolic Nerve cell structural changes
Electrolyte imbalance Metabolic Hyperglycemia Fever Stress Nerve cell structural changes Hypoxia, tumors, trauma

Seizures Classification Generalized Classification Partial
Involves all areas of both cerebral hemispheres Motor manifestations are bilateral Classification Partial Focal onset involving one particular part of the brain

Seizures Status 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

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

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

Seizures Assessment Diagnostic procedures No history
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

Seizures Interventions Pharmacological support to prevent recurrence
Phenytoin, IV Fosphenytoin IV or IM

Seizures Interventions Monitor
Neurological status Temperature, vital signs Pharmacological support to prevent or correct complications 50% glucose IV Thiamine IM or IV

Seizures Interventions Interventions Assess for compliance
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.

Neurological Emergencies

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