Neurologic System

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AACN CCRN Review

Neurologic System

Presenter: Mary Kay Bader RN, MSN, CCRN, CNRN, CCNS, FAHA

Clinical Nurse Specialist Mission Hospital Mission Viejo, CA

Neurologic System

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Adult CCRN Review Neurologic System

Mary Kay Bader RN, MSN, CCRN, CNRN, CCNS, FAHA

Topics o Increased intracranial pressure o Head trauma o Ischemic stroke o Hemorrhagic stroke o Neurologic infectious diseases o Seizures and epilepsy o Status epilepticus o Brain tumors

Increased Intracranial Pressure o Classification

Increases in tissue volume Increases in blood volume Increases in cerebrospinal fluid (CSF) volume Congenital abnormalities Metabolic

o Pathophysiology o Signs/Symptoms Increased Intracranial Pressure (ICP)

Decrease in level of consciousness (LOC) Motor

Contralateral motor deficit Cranial nerves

Ipsilateral pupil abnormalities Headache and/or vomiting Cushing’s triad

Bradycardia Widening pulse pressure Respiratory arrest

o ICP Monitoring Indications for monitoring ICP:

GCS 3 – 8 CT reveals abnormality

o Types of monitoring devices o Intraparenchymal bolt Ventriculostomy

Intracranial pressure Normal: 0‒15 mm Hg

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Elevated: >20 mm Hg

o Cerebral Blood Flow (CBF) CBF – cerebral perfusion pressure (CPP)/cerebrovascular resistance (CVR) CPP = mean arterial pressure (MAP) – ICP

Injured brain optimize CPP Use target of 50–70 mm Hg

o Autoregulation o Cerebral Blood Flow

Autoregulation Vasomotor control

Intact: Increase in CPP causes vasoconstriction and decrease in ICP

Vasomotor reactivity failure: Increase in CPP causes vasodilation and increased ICP Flow metabolism

metabolism CBF Metabolic substances

PaO2

PaCO2

pH—ie, acidosis = vasodilation o Interventions

Head of bed (HOB)/neck positioning Quiet environment Monitor ICU and drain CSF if ICP > 20 mm Hg Airway and breathing

PaO2 and PaCO2

Target PaO2 > 80 mm Hg and PaCO2 35 – 40 mm Hg

Decrease PaCO2 30–35 mm Hg if impending herniation Circulation

Maintain CPP >50–70 mm Hg Maintain euvolemia/vasopressors

Sedation and analgesia as indicated for control of ICP Normothermia

o Secondary Interventions Mannitol

0.25–1 g/kg Replace fluids lost to maintain euvolemia

Hypertonic saline 3%—200 mL over 20 minutes 5%—150 mL over 20 minutes 7%—100 mL over 20 minutes 23.5%—15–20 mL

o Tertiary Interventions Decompressive hemicraniectomy

Large Early

Temperature control Hypothermia for refractory increased ICP

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Barbiturate coma

Uncontrolled Increased ICP: Progression to Brain Death o President’s Commission report on guidelines for determination of brain death

culminated in a legal definition and established the Uniform Determination of Death Act In individual who has sustained either:

Irreversible cessations of circulatory and respiratory functions

Irreversible cessation of all functions of the entire brain

Uncontrolled Increased ICP: Progression to Brain Death o Determining brain death—4 steps

o Establish irreversible and proximate cause of coma

History, examination, neuroimaging, and laboratory o Achieve a normal or near-normal core temperature

> 35⁰ C (as close to 36⁰ C) o Achieve a normal systolic BP >100 mm Hg o Perform one neurologic exam (acceptable in most states)

Some states require more than one exam and some may specify a certain level of expertise (eg, neurologist/neurosurgeon)

o Perform one neurologic exam (acceptable in most states)

Coma: must lack all level of responsiveness (no eye opening, no eye movement, no motor response to stimuli)

Absence of brainstem reflexes (fixed pupils, absent dolls eyes/cold calorics, absent corneal/swallow/gag, and no facial)

Apnea: absence of spontaneous breathing (allow PaCO2 >60 mm Hg) o 8–10 min support with 100% FiO2 via O2 to ET tube

Ancillary tests: EEG, cerebral angio, nuclear scan blood flow o Not used to confirm brain death and cannot replace the clinical exam

o Time of brain death is:

Time the PaCO2 reaches the target level and absent spontaneous breathing

If unable to do apnea, time of ancillary test officially interpreted

Review Questions

Question #1 —A brain-injured patient was admitted 4 hours ago after sustaining a large subdural hematoma (SDH) which was evacuated surgically. AN ICP monitor with CSF drainage was placed by the MD. The ICP increases to 24 mm Hg while the patient’s CPP is 64 mm Hg. After draining CSF, the first intervention would be to lower the ICP by: o Lowering the HOB o Administering hypertonic saline or mannitol o Instituting a pentobarbital coma o Lowering the PaCO2 to 28 mm Hg

Question #1 rationale— A brain-injured patient was admitted 4 hours ago after sustaining a large SDH which was evacuated surgically. AN ICP monitor with CSF drainage was placed by the MD. The ICP increases to 24 mm Hg while the patient’s CPP is 64 mm Hg. After draining CSF, the first intervention would be to lower the ICP by: o Lowering the HOB. Lowering the HOB would increase the ICP o Administering hypertonic saline or mannitol

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o Instituting a pentobarbital coma. Instituting a pentobarbital coma would be a tertiary intervention

o Lowering the PaCO2 to 28 mm Hg. Lowering the PaCO2 to 28 mm Hg would decrease CBF and create ischemia, especially on day 1 of TBI when cerebral blood flow is often critically reduced; this should be avoided

Question #2 —It is day 4 of FZ’s hospitalization following a severe traumatic brain injury (TBI). He has experienced an increase in urine output (1000 mL) over the past 3 hours. His MAP has decreased to 75 mm Hg and his ICP had increased to 30 mm Hg, resulting in a CPP of 45 mm Hg. If FZ has intact autoregulation, the most appropriate intervention would be to: o Administer 500 mL fluid bolus to increase the MAP and decrease the ICP o Administer 50 g of mannitol to reduce the ICP o Begin nicardipine to lower the MAP and ICP o Do nothing, since the MAP/ICP/CPP are within normal ranges

Question #2 rationale—It is day 4 of FZ’s hospitalization following a severe TBI. He has experienced an increase in urine output (1000 mL) over the past 3 hours. His MAP has decreased to 75 mm Hg and his ICP had increased to 30 mm Hg, resulting in a CPP of 45 mm Hg. If FZ has intact autoregulation, the most appropriate intervention would be to: o Administer 500 mL fluid bolus to increase the MAP and decrease the ICP o Administer 50 g of mannitol to reduce the ICP. Administering 50 g of mannitol to reduce the

ICP may significantly lower the BP resulting in a further increase in ICP o Begin nicardipine to lower the MAP and ICP. This would actually increase the ICP o Do nothing, since the MAP/ICP/CPP are within normal ranges. The ICP is elevated (>20 mm

Hg) and the CPP is not in the ideal range of 50–70 mm Hg

Head Trauma Etiology of Brain Injury

o Mechanisms of injury Trauma

Blunt

Penetrating

Blast

Pathophysiology of Brain Injury o Primary injury

Trauma

Skull integrity

Brain integrity o Focal injuries o Diffuse injuries

Classification o Secondary injury r/t event

Cerebral edema Changes in CBF Cellular

Types of Primary Injuries o Scalp

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o Skull

Primary Injuries o Cerebral injuries

Diffuse Focal

Diffuse Injury: Concussion o Stretch injury of axons o Temporary disturbance in neurologic function o Grades 1 – 3 o Post-concussive syndrome

Diffuse Axonal Injury o Shearing

Disruption of axons CT

Degrees of coma Control of ICP Prolonged Recovery varies

Epidural Hematoma (EDH) o Associated with linear skull fracture

Children may not have skull fracture with epidural Rare in older adults

o Location: 75% temporal region o CT: biconvex o Exam o Treatment

Removal of hematoma Post-op monitoring of neurologic status and determining any cognitive deficits

SDH o Associated with high-velocity deceleration o Timing and cause Acute within 24–48 hours

Rupture of bridging cortical veins

Increased ICP/contusions Subacute: 48 hours to 10 days Chronic: 10 days to 6 weeks

Rupture of bridging veins across parasagittal space o CT o Clinical presentation

Acute SDH

Subacute SDH o Subacute SDH

Usually unilateral isodensity 2 -10 days after event

o Chronic SDH Usually bilateral isodensity 2 – 6 weeks after event

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Management of SDH o Acute

Acute surgical decompression Synchronous with increased ICP management

o Subacute and chronic Burr holes for removal of fluid Flat for 1–2 days Gradual elevation of HOB Evaluation for deficits

Cerebral Contusions o Types

Fracture Coup Countercoup Herniation Surface Gliding (focal hemorrhage in cortex/subjacent white matter found in diffuse axonal

injury) o Frequently frontal or temporal regions o Vasogenic edema and central necrosis o Diagnosis: CT and exam

Focal Injury: Cerebral Contusions o Care Priorities

Manage ICP Manage life support systems Assessment of deficits Education of patient/family

Head Injury Assessment o History of event o Severity of injury based on Glasgow Coma Scale (GCS)

Mild 13–15 Moderate 9 –12 Severe 3–8

o Signs of increased ICP and evidence of injury o Diagnostics

Interventions o Airway

Oxygenation: airway and oxygen Ventilation:

Initial: PaCO2 35–45 mm Hg

Phase II (days 2–6): PaCO2 may decrease BP and volume

2007 Brain Trauma Foundation Guidelines: CPP 50–70 mm Hg

Fluids/vasopressors Mannitol or hypertonic saline Positioning

HOB 30⁰ with neck midline

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Interventions o Draining CSF for ICP > 20 mm Hg o Temperature regulation

Keep normothermic (37⁰ C) o Refractory ICP

Decompressive hemicraniectomy Mild hypothermia

o Nutrition o System support o Rehab

Review Questions Question #3—JR, a 34-year-old male, fell from a ladder and sustained a severe TBI. His GCS on

arrival was 1-3-1 with pupils at 2 mm and minimally reactive to light. CT scan of brain shows multiple punctate hemorrhages along with an acute EDH. The neurosurgeon evacuated the bleed and placed an ICP/brain oxygen monitor into the brain. On admission to ICU: GCS 1-4-1; MAP 80 mm Hg; ICP 10 mm Hg; CPP 70 mm Hg, PbtO2 12 mm Hg (normal 20–40 mm Hg); PaCO2 30 mm Hg; CVP 10 mm Hg. What is your first intervention?

o Give 250 mL NS to increase CVP o Administer mannitol g IV push o Decrease the tidal volume or rate to increase the PaCO2 o Do nothing, since the patient’s parameters are within the normal zone

Question #3 rationale—JR, a 34-year-old male, fell from a ladder and sustained a severe TBI. His GCS on arrival was 1-3-1 with pupils at 2 mm and minimally reactive to light. CT scan of brain shows multiple punctate hemorrhages along with an acute EDH. The neurosurgeon evacuated the bleed and placed an ICP/brain oxygen monitor into the brain. On admission to ICU: GCS 1-4-1; MAP 80 mm Hg; ICP 10 mm Hg; CPP 70 mm Hg, PbtO2 12 mm Hg (normal 20–40 mm Hg); PaCO2 30 mm Hg; CVP 10 mm Hg. What is your first intervention?

o Give 250 mL NS to increase CVP. Incorrect; the CVP and CPP are normal o Administer mannitol g IV push. Incorrect; the ICP is normal o Decrease the tidal volume or rate to increase the PaCO2 o Do nothing, since the patient’s parameters are within the normal zone. Incorrect,

because the patient’s oxygen level is critically low in the brain

Question #4—EG, an 80-year old male, was previously independent and able to care for himself. His daughter stated he is now unable to walk and is confused/disoriented. A CT scan of the brain reveals bilateral large chronic SDH. The neurosurgeon evacuated both SDH and has placed a Jackson-Pratt drain to gravity. The patient was extubated post-op. Where should the HOB be maintained? o HOB flat for 24–48 hours o HOB at 15⁰ for 10 days o HOB at 30⁰ to reduce ICP o HOB at 45⁰to reduce ICP

Question #4 rationale—EG, an 80-year old male, was previously independent and able to care for himself. His daughter stated he is now unable to walk and is confused/disoriented. A CT scan

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of the brain reveals bilateral large chronic SDH. The neurosurgeon evacuated both SDH and has placed a Jackson-Pratt drain to gravity. The patient was extubated post-op. Where should the HOB be maintained? o HOB flat for 24–48 hours o HOB at 15⁰ for 10 days. Incorrect, due to the position and length of time o HOB at 30⁰ to reduce ICP. Incorrect because the ICP is usually normal and the brain needs to

re-expand into the space occupied by the blood clot. Typically, elderly individuals undergo significant brain atrophy, and thus have more space in the cranial vault

o HOB at 45⁰to reduce ICP. Incorrect because the ICP is usually normal and the brain needs to re-expand into the space occupied by the blood clot. Typically, elderly individuals undergo significant brain atrophy, and thus have more space in the cranial vault

Stroke Ischemic Stroke

Risk factors Signs/symptoms

FAST

Face, arm, speech, time

Motor weakness

Asymmetrical smile

Difficulty speaking

Numbness

Visual changes

Difficulty swallowing Use NIHSS to assess

Full

Abbreviated Etiology

Thrombotic 20-25%

Embolic 20%

Lacunar 20%

Cryptogenic 30% Pathophysiology

Reduced blood flow

Importance of collateral flow

BP management

Impact of glucose and temperature

Three factors affecting outcomes

Time dependent

Degree of ischemia

Collateral circulation

Pathophysiologic issues related to stroke Edema and increase ICP

Occurs as natural evolution of insult

Minimized if perfusion restored

Assess for change in neurologic status

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Do not medicate with sedation agents unless monitoring for increased ICP

Prepare for CT

Ischemic Stroke Intervention

ABC

Supplemental O2 for SaO2 <94% BP management

Assess BP and Treat

No tPA: SBP >220 mm Hg; DBP >120 mm Hg or MAP >130 mm Hg

tPA: SBP >185 mm Hg or DBP >110 mm Hg

Only use labetalol or nicardipine

Monitoring Neuro exam every 15 minutes x 4 until treatment decision made

IV and labs

Diagnostics CT scan

No hemorrhage

No edema 12-lead ECG: NSR

Ischemic Stroke Time window: candidates for tPA Intravenous tPA

Time window was <3 hours

Time window now moved to 4.5 hours

Scientific Advisory: tPA o tPA should be administered to eligible patients who can be treated in the time period of 3 to

4.5 hours after stroke

Intravenous tPA: Indications o Patient symptoms <4.5 hours from symptom onset

CT scan excludes hemorrhage NIH stroke scale >4 Isolated aphasia Age >18

o Note exclusions for 3– 4.5 hour IV tPA Age >80 years Taking oral anticoagulants NIHSS >25 Combination of history of prior stroke and diabetes

Ischemic Stroke o Decision point

Thrombolysis: up to 6 hours

IV 3–4.5 hours

IV/IA 4.5 hours

IA 6 hours (off label) Merci retrieval/penumbra device/solitaire

Up to 8 hours Supportive care

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Aspirin 325 mg rectally by 48 hours

Infusion Guidelines tPA o Preparation of IV tPA drip

0.9 mg/kg 10% IV over 1–2 minutes 90% IV over 60 minutes

o Administration of tPA Monitor VS: every 15 minutes x 2 hours, every 30 minutes x 6 hours, then every hour x

16 hours Treat BP accordingly

Ischemic Stroke o tPA

BP considerations: treatment

SBP >185 mm Hg/ DBP >110 mm Hg Administration: IV

Postinfusion care: Treat systolic BP >180 mm Hg and diastolic BP >105 mm Hg Supportive care

Do not drop BP unless: o Systolic BP >220 mm Hg/diastolic BP >120 mm Hg o Treat with labetalol or nicardipine

o VS/neuro checks every 1 – 2 hours NIHSS

o Support airway/O2/pulse oximetry o Cardiac telemetry o HOB flat vs 30⁰

Flat if no signs of increased ICP – supports improved flow HOB 30⁰ if signs of increased ICP

o NPO until swallow assessment o Temperature management

Treat temperature >98.6⁰ F o Hydrate/control serum glucose <180 mg/dL o Observe neurologic status o Medications: statins and antiplatelet agents o Begin nutrition o Early mobility o Prevent complications

Aspiration: NPO until swallow assessment DVT UTI

o Educate family o Secondary stroke prevention

Review Questions Question #5—LL, a 65-year-old female, developed an acute onset of left-sided weakness with

neglect to the left side at 12:35 PM. Her speech became slurred and she didn’t know where she was. LL’s son brought her to the ED, where a CT scan of the brain revealed no hemorrhage. A CTA demonstrated an occlusion of the right middle cerebral artery. The ED physician/neurologist

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has ordered IV tPA. It is 2 hours, 50 minutes since symptom onset. The patient’s last BP was 190/100 mm Hg. Your first action is: o Administer the tPA 0.9 mg/kg IV dose because there is only 10 minutes in the treatment

window o Administer the tPA 0.6 mg/kg IV dose and labetalol 10 mg IVP at the same time o Start IV nitroprusside to reduce the BP o Administer 10–20 mg IV labetalol to reduce the BP prior to administering the tPA

Question #5 rationale—LL, a 65-year-old female, developed an acute onset of left-sided weakness with neglect to the left side at 12:35 PM. Her speech became slurred and she didn’t know where she was. LL’s son brought her to the ED, where a CT scan of the brain revealed no hemorrhage. A CTA demonstrated an occlusion of the right middle cerebral artery. The ED physician/neurologist has ordered IV tPA. It is 2 hours, 50 minutes since symptom onset. The patient’s last BP was 190/100 mm Hg. Your first action is: o Administer the tPA 0.9 mg/kg IV dose because there is only 10 minutes in the treatment

window. Incorrect because controlling the BP must be done prior to administering tPA o Administer the tPA 0.6 mg/kg IV dose and labetalol 10 mg IVP at the same time. Incorrect

because the dose of tPA is incorrect and the BP must be lowered prior to the administration of tPA

o Start IV nitroprusside to reduce the BP. Incorrect because labetalol and nicardipine are the first two drugs of choice when lowering BP in acute stroke

o Administer 10–20 mg of IV labetalol to reduce the BP prior to administering the tPA

Question #6 —BP, a 90-year-old female, presents with acute onset of aphasia and right-sided hemiparesis. She was last seen normal 12 hours ago. Her PT 195/105 mm Hg. Which medication do you anticipate the physician team to order first? o Labetalol 10 mg IV to lower the BP o tPA 0.9 mg IV (10 % IV bolus/90% drip over 60 minutes) o Aspirin 325 mg PO o Aspirin 325 mg per rectum

Question #6 rationale—BP, a 90-year-old female, presents with acute onset of aphasia and right-sided hemiparesis. She was last seen normal 12 hours ago. Her PT 195/105 mm Hg. Which medication do you anticipate the physician team to order first? o Labetalol 10 mg IV to lower the BP. Incorrect because the BP threshold in the non-tPA

patient is 220/120 mm Hg o tPA 0.9 mg IV (10 % IV bolus/90% drip over 60 minutes). Incorrect since the patient

symptoms are >4.5 hours o Aspirin 325 mg po. Incorrect since the patient may have difficulty swallowing and needs to

have her swallow evaluation prior to receiving any oral medications o Aspirin 325 mg per rectum

Hemorrhagic Stroke

Intracerebral Hemorrhage (ICH) o Usually a result of hypertension o Releases toxins that leads to vasospastic activity o Local decrease in perfusion o Global decrease in perfusion

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o Cellular changes

SAH: Aneurysm o Aneurysms o Occur at bifurcation o Defect in artery o Rupture point o Bleeds into subarachnoid space, brain tissue or ventricles o Danger

Rebleeding Vasospasm

Vascular Malformations o Developmental vascular anomalies o Result from error in embryonic vascular network o 86% of all SAH

Only 1% of all strokes Ratio of AVM to aneurysm 1:10

o Symptom onset 80% between 20–40 years of age 20% before age 20

Pathophysiology : Ruptured AVM o Rupture causes hemorrhage, increased ICP, and hemispheric damage

Hemorrhagic Stroke o Assessment: ICH

Headache, altered LOC, and nausea/vomiting Motor weakness and sensory changes Cranial nerve deficits Signs of increased ICP

o Assessment: SAH “Worst headache of life” Meningeal: photophobia and nuchal rigidity Nausea/vomiting and dizziness Focal deficits, ie, 3rd nerve

o Aneurysms—Assessment grading: Hunt and Hess scale I: alert, no deficit, and minimal headache II: awake, CN palsy, mild to severe headache III: drowsy, confusion, and mild focal deficit IV: unresponsive and hemiplegia V: comatose, moribund, and extensor posturing

o Diagnostic work-up Lumbar puncture

Presence of RBCs/WBCs

Elevated protein CT scan

Presence of SAH Angiogram Spiral CT angiogram MRI/MRA

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o Management of ICH Medical management of ICH

Surgery vs medical management vs palliative care

Ventriculostomy and ICP monitoring Team Management

ABC

Airway/ventilation

BP control

Circulation: Normovolemia and VTE prophylaxis ICP control: CSF drainage and mannitol vs hypertonic saline bolus

System support o Management of SAH

Pre-op

BP control (SBP < 140 – 15 mm Hg)

Frequent assessments to monitor for neurologic deterioration due to hydrocephalus or rebleeding

Surgical clipping vs coiling o Team management of SAH

Pre-op Post-op

ABC:

PaO2 >80 mm Hg PaCO2 >35 mm Hg

Watch for myocardial stunning

Target BP 120 – 15 mm Hg unless vasospasm present

ICP control: CSF drainage

Vasospasm Most likely days 4 - 14 o BP management and double H therapy

Keep BP normalized until vasospasm begins If vasospasm, then elevate BP

o Nimodipine o Watch for change in exam and/or sodium drop and diuresis

Interventions o NG o IV fluids o Maintain anticonvulsants o Examine patient for injury o Treat hyperthermia o Begin nutrition o Early mobility o Psychological support

Review Questions

Question #7—SS, a 50-yearl-old female, presents with the worst headache of her life and photophobia. Her neuro exam is otherwise normal. CT scan of brain shows a large SAH from a possible cerebral aneurysm. Her BP is 170/100 mm Hg. Initially, the physician will want the BP treated if: o Systolic BP >90 mm Hg

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o Systolic BP >150 mm Hg o Systolic BP >180 mm Hg o Systolic BP >220 mm Hg

Question #7 rationale—SS, a 50-year-old female, presents with the worst headache of her life and photophobia. Her neuro exam is otherwise normal. CT scan of brain shows a large SAH from a possible cerebral aneurysm. Her BP is 170/100 mm Hg. Initially, the physician will want the BP treated if: o Systolic BP >90 mm Hg. A SBP <90 mm Hg would not be beneficial to cerebral perfusion o Systolic BP >150 mm Hg o Systolic BP >180 mm Hg. This range is too high and may contribute to rebleeding of the

aneurysm o Systolic BP >220 mm Hg. This range is too high and may contribute to rebleeding of the

aneurysm

Question #8—BP, a 52-year old female, was admitted to the ICU following rupture of a cerebral aneurysm and large SAH. CT scan of her brain revealed acute hydrocephalus. The most likely cause of BP’s hydrocephalus is: o Cerebral aneurysm exerting pressure on the choroid plexus in the ventricles, limiting the CSF

absorption o Blood in subarachnoid space mixing with CSF and occluding the arachnoid villi, which helps

reabsorb CSF in the brain o Overproduction of CSF from the aneurysm rupture o Reduced absorption of CSF by the choroid plexus

Question #8 rationale—BP, a 52-year old female, was admitted to the ICU following rupture of a cerebral aneurysm and large SAH. CT scan of her brain revealed acute hydrocephalus. The most likely cause of BP’s hydrocephalus is: o Cerebral aneurysm exerting pressure on the choroid plexus in the ventricles, limiting the CSF

absorption. The choroid plexus makes CSF. It does not absorb CSF o Blood in subarachnoid space mixing with CSF and occluding the arachnoid villi, which

helps reabsorb CSF in the brain o Overproduction of CSF from the aneurysm rupture. Aneurysmal rupture does not increase

CSF production by the choroid plexus o Reduced absorption of CSF by the choroid plexus. CSF is absorbed by the arachnoid villi

Question #9—SS is now 10 days post aneurysm rupture. The aneurysm was surgically clipped on day 2. SS began complaining of a headache this morning. Her motor exam has changed in the last 2 hours with her right arm motor strength has diminished from 5/5 to 3/5. She is having word-finding problems with her speech. The most likely explanation for this change in status is: o Increased ICP

o Rebleeding

o Ischemic stroke

o Vasospasm

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Question #9 rationale—SS is now 10 days post aneurysm rupture. The aneurysm was surgically clipped on day 2. SS began complaining of a headache this morning. Her motor exam has changed in the last 2 hours with her right arm motor strength has diminished from 5/5 to 3/5. She is having word-finding problems with her speech. The most likely explanation for this change in status is: o Increased ICP. Although cerebral edema is possible after SAH, a change in LOC should occur

o Rebleeding. Since the aneurysm has been surgically repaired, this complication is unlikely

o Ischemic stroke. If vasospasm is not treated, the end result could be an ischemic stroke

o Vasospasm

Neurologic Infectious Diseases

Meningitis

o An inflammation of the meninges

o Primary causes

Bacterial

Viral

Fungal

Other causes include parasites and cancer

Meningitis: Causative Agents

Bacterial Viral Fungal

Streptococcus

pneumonia

Neisseria meningitides

Haemophilus influenza

Group B streptococcus

Escherichia coli

Listeria monocytogenes

Mycobacterium

tuberculosis

Treponemia pallidum

(neurosyphilis)

Enteroviruses:

Coxsackieviruses

Echoviruses

Polioviruses

Arborviruses:

Transmitted by arthropod

vectors (mosquitos or ticks)

(eg, St. Louis encephalitis)

Other:

Mumps virus; measles virus;

rubella virus; lymphocytic

choriomeningitis virus; HIV;

herpesvirus, including herpes

simplex virus; varicella-zoster

virus, cytomegalovirus, and

Epstein-Barr

Cryptococcus

neoformans

Coccidiodes immitis

Candida albicans

Blastomyces dermatitidis

Histoplasma capsulatum

Paracoccidiodes

brasiliensis

Sporothrix schenckii

Pseudallescheria boydii

Aspergillus fumigates

Meningitis

o Pathophysiology

Access routes: open wound, mucous membrane, or infected tissue

Direct

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Penetrating wounds, skull fractures, neuro operative procedures, LPs, ICP, otitis

media, sinusitis, or osteomyelitis

Hematogenous

Septicemia/bacteremia, septic emboli, bacterial endocarditis, URI, pelvic

abscess

CSF leak: rhinorrhea/otorrhea

Meningitis

o Pathophysiology

Bacterial process

Colonization: invades tissue/gains access to blood

Crosses blood‒brain barrier

No host immune defense in CSF

Rapid replication of bacteria

Rapid increase in neutrophils

Lysis of bacteria

Produces exudate and inflammation of meninges

Cerebral edema, vasculitis, infarctions, hydrocephalus, and increased ICP

Bacterial Meningitis: Assessment

o Subjective data

Varies depending upon the pathogen

Headache, neck or back pain, photophobia, and malaise

o Objective data

Clinical triad: fever, nuchal rigidity, altered mental status

Meningeal irritation: headache, nuchal rigidity, photophobia, Kernig’s sign, and Brudzinski’s sign

o Kernig’s sign

Patient supine

Flex hip 90⁰

Straighten leg = pain in hamstring

Bacterial Meningitis: Objective Data o Focal neurological deficits: cranial nerve palsies (CN II – CN VIII), diplopia, seizures,

hemiparesis, and altered mental status o Petechial rash

Occurs 50% of meningococcal cases

Tiny red or purple pinprick rash that progresses to purple blotches, located on trunk, lower extremities, mucous membranes, and conjunctiva

Poor outcome with rapidly evolving rash and requires emergent care

Tumbler test Similar rashes observed in pneumococcal, H influenzae, and enteroviral meningitis

o Nausea, vomiting, chills, malaise, pain in the back, abdomen, and extremities

Bacterial Meningitis: Diagnostics o Medical history and clinical exam o Laboratory studies

Chemistry and coagulation profile, cultures, CSF studies, serology o CT/MRI of the head

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o Lumbar puncture

Contraindications: ICP, CNS mass lesion, focal neurological deficits, papilledema, coagulation disorders, meningococcal septicemia, or septic shock

o Radiography: chest and sinus o EEG

Meningitis o Data assessment—diagnostics

Cultures, cells, glucose protein

Normal CSF Bacterial Viral Fungal

WBC cells/mm

0-5 cells 1000-5000 50-1000 >20

Neutrophils 0% >80% <40% 0

Protein mg/dL 18-45 100-500 <200 >45

Glucose mg/dL 45-80 (0.6xBS) 5-40 (<0.3xBS) >45 <40

Bacterial Meningitis: Patient Problems o Infection of meninges o Elevated body temperature r/t CNS inflammation o Acute pain r/t inflammation of meninges, headache, nuchal rigidity, irritation of pain

receptor, or ICP secondary to CNS inflammation o Seizures: risk for injury r/t seizure activity secondary to cerebral irritation o Increased ICP r/t CNS infection o Hydrocephalus r/t CNS inflammation o Respiratory complications: risk for ineffective respiratory function r/t immobility and pain,

ineffective airway clearance, risk for aspiration r/t seizure activity

Bacterial Meningitis: Infection of Meninges o Characteristics: pain, meningeal irritation, petechial rash o Medical interventions

Antibiotic therapy Strep pneumonia: pen G, ceftriaxone, cefotaxime Resistant to pen—vancomycin Neisseria: pen G or ampicillin H flu: cefotaxime or ceftriaxone

Corticosteroid therapy o Surgical interventions

Treat complications—eg, drainage of CNS abscesses or insertion of ventricular-peritoneal shunt for communicating hydrocephalus

o Nursing interventions

Droplet precautions

Vital signs

Neuro checks

Monitor lab results

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Administer antibiotics, antipyretics, analgesics, and IV fluids

Provide quiet, darkened room and encourage rest

Bed rest, neutral alignment

Promote nutritional intake and fluids

Provide skin care o Expected outcomes

Infectious source identified and infection successfully treated

Return to prior baseline status

No residual neurological deficits

Remains seizure-free o Potential complications

Waterhouse-Friderichsen syndrome

DIC

Sensori-neural hearing or vision loss

Encephalitis or hydrocephalus

Brain abscess or subdural effusions

Increased ICP cerebral herniation death

Permanent neurological deficits

Paralysis; ARDS

Seizures

Bacterial Meningitis: Increased ICP r/t CNS Infections o Characteristics

Change in neurological status

Altered vital signs

Cranial nerve deficits

Headache, nausea, vomiting, dizziness, or nuchal rigidity

Hydrocephalus o Medical interventions

Hyperosmolar diuretics: mannitol

Hypertonic saline

Sedatives: propofol or benzodiazepines

Narcotics: fentanyl or morphine

Fluid administration: crystalloids or colloids o Surgical interventions

Insert ICP monitoring device or external ventricular drain Maintain ICP <15 mm Hg and CPP >60 mm Hg

Perform surgical decompression, excise or drain abscess or lesion to relieve pressure

Ventricular peritoneal shunt placement for hydrocephalus management

Bacterial Meningitis: Increased ICP r/t CNS Infections o Nursing interventions

Monitor neurological status and vital signs

Elevate HOB 30⁰

Suction as needed

Monitor ICP and EVD

Maintain euvolemia, normothermia, and normal electrolyte levels

Administer stool softeners to avoid Valsalva maneuver

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Maintain quiet, darkened room with minimal stimulation o Expected outcomes

ICP remains <15 mm Hg and CPP >60 mmHg or as ordered

Neurological status improves or baseline is maintained

Complications of ICP are resolved

No complications of ICP monitoring develop o Potential complications

Complications of ICP monitoring: fever, infection, seizures, excess fluid volume, herniation, and death

Bacterial Meningitis: Elevated Body Temperature r/t CNS Inflammation o Characteristics

Fever

Warm flushed skin

Diaphoresis

Tachycardia

Tachypnea

Seizures o Medical interventions

Antipyretics

Cooling devices o Nursing interventions

Administer antipyretics as necessary

Administer IV fluids as ordered

Monitor intake and output

Institute cooling measures

Monitor vital signs

Monitor level of consciousness

Monitor lab values: WBC and electrolytes

Bacterial Meningitis: Elevated Body Temperature r/t CNS Inflammation o Expected outcomes

Patient remains afebrile at 37⁰ C

Patient’s BP, RR, and HR are WNL

Patient remains seizure-free o Potential complications

Seizures

Activity intolerance r/t fatigue and malaise secondary to infection

Delayed growth and development r/t brain damage secondary to infectious process, ICP

Disturbed sensory perception: impaired auditory, kinesthetic, visual acuity r/t CNS infection

Bacterial Meningitis: Acute Pain r/t Inflammation of Meninges, Headache, Nuchal Rigidity, Irritation of Pain Receptors, or ICP Secondary to CNS Inflammation o Characteristics

C/o headache, neck and back pain, or nuchal rigidity

Guarding or protective behavior

Withdrawal from social contact

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Facial mask of pain

Moaning, crying, irritability

Increase in vital signs, restlessness o Medical interventions

Analgesic medications as necessary

Supportive therapy o Nursing interventions

Assess location, quality, severity of pain

Assess patient behavior and physiological signs secondary to pain

Provide quiet, darkened room with minimal disturbances

Implement comfort measures to promote relaxation

Institute nonpharmacological measures for pain control

Administer analgesics as prescribed

Assess patient’s pain and effectiveness of interventions and side effects

Administer pain medication prior to activities

Bacterial Meningitis: Acute Pain r/t Inflammation of Meninges, Headache, Nuchal Rigidity, Irritation of Pain Receptors, or ICP Secondary to CNS Inflammation o Expected outcomes

Patient reports adequate pain control

Vital signs are WNL o Potential complications

Risk for injury r/t restlessness and disorientation secondary to pain

Bacterial Meningitis: Seizures Risk for Injury r/t Seizure Activity Secondary to Cerebral Irritation o Characteristics

Loss of consciousness

Incontinence of bowel and bladder

Profuse salivation

Apnea and cyanosis

Respiratory and metabolic acidosis o Medical interventions

Antiepileptic medications

Sedation o Expected outcomes

Patient remains seizure-free

No injuries occur during seizure

No toxic side effects from antiepileptic medications o Nursing interventions

Implement seizure precautions

Protect patient from injury

Document seizure activity

Monitor neurological status and vital signs after seizure

Administer antiepileptic medications as ordered o Potential complications

Status epilepticus

Injury

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Respiratory compromise secondary to ineffective airway clearance

Bacterial Meningitis: Hydrocephalus r/t CNS Inflammation o Characteristics

Headache, N/V

Lethargy

Visual disturbances

Ataxia

Incontinence o Surgical interventions

EVD

Ventricular peritoneal shunt o Nursing interventions

Monitor neurological status and vital signs

Maintain EVD

Provide ventricular shunt post-op care

Monitor for signs of shunt malfunction o Expected outcomes

Hydrocephalus is relieved

Shunt insertion post-op recovery is unremarkable

Shunt functions properly o Potential complications

ICP leading to cerebral herniation and death

Shunt malformation

Viral Meningitis

o Pathophysiology

Viral transmission: fecal–oral contamination or respiratory droplets

Virus replicates at site of entry

Primary viremia is followed by viral replication in blood and spread to CSF

Patient is infectious from 3 days after infection to 10 days after symptoms develop

Incubation period 3–7 days

o Data assessment: Neurologic Exam

Viral

Milder than bacteria

Resembles influenza

Headache, fever, photophobia, malaise, and nausea

Viral Meningitis: Patient Problems o Infection of meninges o Elevated body temperature r/t CNS inflammation o Acute pain r/t CNS inflammation o Hydrocephalus r/t meningitis o GI complications r/t inadequate nutrition o Impaired mobility r/t CNS infection o Psychosocial anxiety r/t CNS infection

Viral Meningitis: Infection of the Meninges o Characteristics

Headache

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Neck pain

Back pain o Medical interventions

Empiric antibiotic therapy initiated until bacterial cultures negative

Acyclovir (Zovirax) used to treat herpes virus types 1 & 3 and varicella-zoster virus

Supportive therapy o Nursing interventions

Same as for bacterial meningitis o Expected outcomes

Patient recovers without neurological sequelae o Potential complications

Encephalitis

Hydrocephalus

Cerebral edema with ICP

Fungal Meningitis o All major fungal agents can produce meningitis o Cryptococcus neoformans most common o High-risk groups include immunocompromised persons, especially with HIV infection o Medical: C neoformans meningitis is treated with amphotericin B and flucytosine o Pathophysiology same as bacterial meningitis

Fungal Meningitis: Assessment o Clinical manifestations

Clinical symptoms often nonspecific but include: Headache Fever Photophobia Malaise Nausea

Different symptoms in patient with and without HIV infection o Diagnostics

Laboratory studies CSF studies Serology (antigen tests)

India ink examination

Latex agglutination tests

ELISA to isolate fungi in CSF CT or MRI

Identify focal lesions; especially in C. neoformans

Fungal Meningitis: Patient Problems o Infection of meninges o Elevated body temperature r/t CNS inflammation o Acute pain r/t CNS inflammation o Hydrocephalus r/t meningitis o GI complications r/t inadequate nutrition o Impaired mobility r/t CNS infection o Psychosocial anxiety r/t CNS infection

Fungal Meningitis: Infection of the Meninges

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o Characteristics

Pain: Headache, neck and back

Fever, malaise, nausea

Lethargy, personality changes

Cranial nerve palsies, papilledema

Meningismus: headache, nuchal rigidity, photophobia, Kernig’s and Brudzinski’s sign o Medical interventions

Antifungal therapy C neoformans treated with amphotericin B and flucytosine

Supportive therapy o Nursing interventions

Same as for bacterial meningitis o Expected outcomes

Infectious source is identified and infection successfully treated

Returns to prior baseline status

Patient does not experience any permanent neurological deficits

Patient remains seizure-free o Patient complications

Encephalitis

Hydrocephalus

Cerebral edema with ICP

Encephalitis o Definition

Inflammation of the brain parenchyma caused by virus, bacterium, fungus, or parasite o Etiology

Virus is most common cause

Respiratory system: mumps, measles, varicella virus

Oral: enteroviruses/polio

Oral or genital: herpes simplex

Bites Animal: rabies Insect: arbovirus (mosquito) Lyme disease (tick)

o Pathophysiology

Arbovirus: includes St. Louis, eastern, western equine and West Nile virus Humans bitten by the vector are asymptomatic or develop vague flu-like symptoms Produces diffuse disintegration of single nerve cells, inflammation, and necrosis of

both white/gray matter (spares the brainstem) o Pathophysiology

Virus Enters body and colonized Penetrates cell Transcribes virus-coated proteins and replicates the viral nucleic acid Blood‒brain barrier prevents virus from entering CNS but can enter through

cerebral capillaries or choroid plexus and/or along peripheral nerves Virus attacks susceptible neurons and causes sell lysis

Encephalitis: Assessment o Subjective data

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Symptoms vary with organism and area involved

Headache is usually present o Objective data

Signs Fever Nuchal rigidity Photophobia Altered LOC Focal neurological deficits Aphasia Badinski’s reflex Involuntary movements Cranial nerve deficits New psychiatric symptoms Cognitive deficits Seizures

Encephalitis: Diagnostics o Medical history and clinical exam o Laboratory studies

Cultures: blood urine, stool, nasopharynx, or sputum

CSF studies Cell count, cytological characteristics, culture Protein level slightly elevated Glucose level normal PCR

Serology: Elisa & Serological assays for antiviral IgM and IgG o EEG o MRI: if not possible, CT of head with and without contrast o Surgery: tissue biopsy in some cases

Encephalitis: Patient Problems o Infection of the CNS o Elevated body temperature r/t CNS inflammation o Acute pain r/t CNS inflammation o Seizures r/t CNS irritation o Increased ICP r/t CNS inflammation o Respiratory complications o Cardiovascular complications o GI complications r/t inadequate nutrition o Impaired mobility r/t CNS infection o Psychosocial anxiety r/t CNS infection

Encephalitis: Herpes Simplex (HSV) o Most common and most severe form

Herpes simplex virus-1 o 2000 cases annually in USA o 30%–70% mortality rate, neurological deficits o HSV accounts for >50% in patients with HIV o No geographical or seasonal pattern

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HSV Encephalitis: Pathophysiology o HSV lies dormant within dorsal ganglia of trigeminal nerve in 90% of people in USA o Virus is activated in trigeminal ganglia and follows fibers and attacks frontal and temporal

lobes, causing bilateral hemorrhagic necrosis

HSV Encephalitis: Assessment o Subjective data

Headache

Confusion

Hallucinations o Objective data

Change in LOC

Personality and behavioral changes

Memory loss

Aphasia

Hemiparesis

Temporal-lobe seizures

Progression to deep coma as cerebral edema increases, herniation may occur leading to death

HSV Encephalitis: Diagnostics o Lumbar puncture

Elevated open pressure

CSF studies: presence of lymphocytes, increased protein level, normal glucose level

PCR: positive for HSV-1 antigen in 98% of cases o EEG

High-voltage, sharp waves in temporal areas

Slow-wave complexes at regular 2- to 3-second intervals o CT

Normal initially

Later scans show gyral enhancement, hypodensity in temporal areas and mass effect in up to 65% of patients

o MRI

PCR: positive for HSV-1 antigen in 98% of cases

Edema and hemorrhage over inferior portion of frontal and temporal lobes

BBB abnormalities seen with contrast o Surgery to obtain cultures of cerebral tissue

HSV Encephalitis: Patient Problems o Infection of brain parenchyma o Acute pain r/t CNS inflammation o Seizures r/t CNS irritation o Increased ICP r/t CNS inflammation o Respiratory complications o Cardiovascular complications o GI complications r/t inadequate nutrition o Impaired mobility r/t CNS infection o Psychosocial anxiety r/t CNS infection

HSV Encephalitis: Infection of the Brain Parenchyma o Characteristics

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Headache, confusion, hallucinations

Change in LOC

Personality changes, behavioral abnormalities

Focal neurological deficits—aphasia, hemiparesis

Temporal lobe seizures o Medical interventions

Acyclovir within 4 days

Supportive care C neoformans treated with amphotericin B and flucytosine

Supportive therapy o Nursing interventions

Same as for bacterial meningitis o Expected outcomes

Infectious source identified and infection successfully treated

Return to prior baseline status

Patient does not experience any permanent neurological deficits

Patient remains seizure-free

Patient does not experience personality/behavioral changes o Potential complications

Moderate to severe neurological deficits in 50% of survivors

Personality/behavioral changes

Seizures and cognitive disability

ICP leading to cerebral herniation

Mortality rate 28% at 18 months after treatment

HSV Encephalitis: Outcomes o Life-threatening illness o Mortality rate of 30%–70% o Increased age and LOC usually predict poor outcomes

Guillain-Barré Syndrome o Definition

Acute, inflammatory, demyelinating polyneuropathy causing weakness, sensory loss, and areflexia

o Etiology

Immune-mediated with precipitating factors of possible infection (viral 1-2 weeks preceding 70% of all cases)

o Pathophysiology

Inflammatory lesions through peripheral nervous system

Defect linked to peripheral nerve myelin

Some cases cause axonal degeneration

Macrophages attack normal myelin, produce demyelination o Subjective data

Rapidly progressing weakness or paresthesias

Usually ascending o Objective data

Progressive motor weakness which ascends

Sensory loss may not be present

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Loss of DTRs

Facial, ocular, or oropharyngeal muscles affected in 50% of cases

Autonomic dysfunction causing ileus, hypotension, hypertension, and arrhythmias

Respiratory compromise if ascends to diaphragm o Diagnostics

LP: increased protein

EMG: slowing of conduction o Management—medical

Plasma exchange urgent every day for 10–15 days

IVIG 1–2 mg/kg in divided doses over 3–5 days Watch for anaphylaxis, chills, fluid overload

Pulmonary—may need to be intubated

Hemodynamic support

Analgesic support for increased pain o Management—nursing

Assess VS/neuro function watching for ascending weakness

Mechanical ventilation—support respiratory function

Watch for hemodynamic alteration Support BP

Assess pain and provide analgesia

Review Questions

Question #10—SP, a 20-year-old college student, presents to the ED with c/o photophobia, stiff neck, temperature of 103⁰, malaise, and purple blotches primarily located on the trunk. He is given antibiotics in the ED. He is admitted to the ICU with a BP of 85/50 mm Hg, HR 140 and ventilated. Cultures have been done but there are no results. SP’s likely infectious illness is: o Lyme disease o Herpes simplex encephalitis o Neisseria meningitides o Guillain-Barré syndrome

Question #10 rationale—SP, a 20-year old college student, presents to the ED with c/o photophobia, stiff neck, temperature of 103⁰, malaise, and purple blotches primarily located on the trunk. He is given antibiotics in the ED. He is admitted to the ICU with a BP of 85/50 mm Hg, HR 140 and ventilated. Cultures have been done but there are no results. SP’s likely infectious illness is: o Lyme disease. Lyme disease is a viral encephalitis that presents with bull’s eye rash and

malaise. It is not accompanied by purple blotches o Herpes simplex encephalitis. The patient may experience headache, fever, malaise but also

has strange behavior, personality changes and seizures o Neisseria meningitides o Guillain-Barré syndrome. Presentation includes ascending weakness accompanied by

sensory loss and cranial nerve dysfunction

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Question #11—Patients sustaining Guillain-Barré syndrome are most likely to have prolonged failure of which organ system? o Cardiac o Respiratory o Renal o Liver

Question #11 rationale—Patients sustaining Guillain-Barré syndrome are most likely to have prolonged failure of which organ system? o Cardiac. Although patients may experience autonomic dysfunction with accompanying BP

variation, arrhythmias, ileus, diaphoresis or loss of sweating, urine retention, it is not chronic heart failure

o Respiratory o Renal. Patients may experience urinary retention but typically do not have acute renal

failure o Liver . The liver is not generally involved

Seizures and Epilepsy Seizures and Epilepsy

o Abnormal firing in the brain o Epileptogenesis occurs during an imbalance between cerebral excitation and inhibition

Brain cells become abnormally linked together, leading to abnormal electrical firing Excitation (glutamate/NMDA) vs inhibition (GABA—facilitates activity of Cl

channels/opens K channels or closes Ca channels) o Classification

Partial seizure: onset of synchronous cortical discharges involving a focal brain region Generalized seizure: sudden onset involving both hemispheres

Seizures and Epilepsy o Partial seizures

Simple partial: focal brain region activity without alteration in consciousness

An aura can be a simple partial seizure

Motor events such as face twitching/hand jerking

Somatosensory events such as unusual taste in mouth

Psychic events—illusions/hallucinations/déjà vu Complex partial seizure: brain region affected with alteration in consciousness

Often preceded by simple partial seizures with progressive impairment in consciousness

Automatisms (lip smacking/blinking/picking at clothes)

Motor phenomena: wandering, running, arm jerking Partial seizure that secondarily generalize

Seizures and Epilepsy o Generalized seizure‒both hemispheres

Absence seizure: impaired responsiveness, minimal motor involvement. Lasts <30 seconds

Myoclonic: sudden shock-like muscle contraction Atonic: drop attacks (brief loss of consciousness/loss of muscle tone) Tonic: increased tone in extensor muscle Clonic: starts with loss of consciousness/sudden hypotonia, then limb jerking

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Tonic-clonic: Loss of consciousness, increased tone, rhythmic muscle jerks

Seizures and Epilepsy o Subjective

Obtain description of event including time Precipitating factors? Post-ictal behavior

o Objective Assess mental state and cognition Evidence of trauma/infection Focal findings Asymmetries

o Diagnostics Lab tests EEG CT/MRI to r/o mass or lesions

Seizures and Epilepsy: Nursing Assessment o History o Type of seizure activity

Absence (petit mal) Focal Tonic-clonic Electrical status Status

Seizures and Epilepsy: Diagnostics o Lab

Electrolytes Hypoglycemia Hypoglycemia Hypoxemia Prolactin level Myoglobin Anticonvulsant drug levels

o EEG

Treatment: pharmacologic Drug Level o Phenobarbital 60-250 mg/day 15-40 mcg/mL o Dilantin (phenytoin) 300-600 mg/day 10-20 mcg/mL o Tegretol (carbamazepine) 600-1200 mg/day 4-12 mcg/mL o Mysoline (primidone) 25 mg tid 5-12 mcg/mL o Depakote (valproic acid) 15-60 mg/kg/day 50-100 mcg/mL o Lamictal (lamotrigine100-300 mg/day 2-4.5 mcg/mL o Neurontin (gabapentin) 900-3600 mg/day 2-20 mcg/mL o Keppra (levetiracetam) 1000-3000mg/day 3-37 mcg/mL o Vimpat (lacosamide) 10-400 mg/day 3.8-9.3 ng/mL

Seizures and Epilepsy o Side-effects profile

Stevens Johnson syndrome: erythema multiforme Aplastic anemia Allergic dermatitis

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Hepatic failure Most common: somnolence, dizziness, memory impairment, cognitive slowing, ataxia

o Nursing interventions Education Explain drug‒drug interactions Other: ketogenic diet (high- fat/low-carb/restrict calories); vagal nerve stimulator;

surgery (temporal lobectomy or corpus callosotomy)

Status Epilepticus

Pathophysiology o Tonic –clonic seizures o Increase cerebral metabolic rate/oxygen use o CBF increases 3–5x normal o Cellular swelling o Systemic metabolic acidosis

Etiology/Precipitating Factors o Withdrawal from anticonvulsants, alcohol, or drugs o CNS infections o Brain tumors o Metabolic disorders—uremia, hypoglycemia, or hyponatremia o Craniocerebral trauma o Cerebral edema o Stroke

Interventions o Airway and ventilation

Supplemental oxygen and pulse oximetry Intubate if prolonged seizure Check blood glucose

o Normal saline IV Thiamine 100 mg diluted with 8 mL NS slow IV push over 5 minutes then 50% dextrose 50 mL slow IV push (if bedside, glucose <70 mg dL)

o Stop seizure Lorazepam 2 mg IV push every 1 minute up to 8 mg Fosphenytoin (Cerebyx) 20 (phenytoin equivalents [PE]) mg/kg

o Protect from injury

Interventions o If still seizing

Give fosphenytoin 5 PE mg/kg IV; may repeat with another dose to a loading dose of 30 PE mg/kg

Phenobarbital 20 mg/kg IV—infuse at 50–100 mg/min; may repeat with additional 5–10 mg/kg to a total dose of 30 mg/kg (must be intubated and mechanically ventilated)

Lorazepam 2 mg/kg V push every 1 minute until a 20 mg total loading dose is given o Additional antiepileptic drug

Valproate sodium (Depacon) 25 mg/kg IVPB loading dose over 60 min x 1 and maintenance 10–15 mg/kg/day every 6 hours

Propofol 1–2 mg/kg x 1 IV (administered by MD), then drip 20–250 mcg/kg/min (must be intubated and mechanically ventilated)

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Pentobarbital 5–15 mg/kg IV x 1 over one hour, then 0.5–3 mg/kg/hr (must be intubated and mechanically ventilated)

Midazolam 10 mg IVP x 1, then 0.05–0.4 mg/kg/hr Diazepam 0.15 mg/kg up to 10 mg IV push at 5 mg/min Lorazepam 2 mg IV push every 2 hours

o No paralytics unless continuous EEG in place

Review Questions Question #12—A 10-year old male ignores repeated requests to answer questions and often

stares for short periods of time, as reported by his teacher. This type of seizure is a: o Partial seizure o Complex partial seizure o Myoclonic seizure o Generalized seizure known as an absence seizure

Question #12 rationale— A 10-year old male ignores repeated requests to answer questions and often stares for short periods of time, as reported by his teacher. This type of seizure is a: o Partial seizure. Partial seizures are localized to one area of the brain and do not impair

consciousness o Complex partial seizure. These are manifested by automatisms and motor phenomena such

as wandering, running, or arm jerking o Myoclonic seizure. These are generalized seizures that are sudden shock-like muscle

contractions o Generalized seizure known as an absence seizure

Question #13—A patient in status epilepticus must receive medication immediately to halt the seizure activity. The first-line medication for status epilepticus is: o Diazepam 10 mg PO o Midazolam 1 mg IV o Phenobarbital 30 mg IV o Lorazepam 2 mg IV

Question #13 rationale—A patient in status epilepticus must receive medication immediately to halt the seizure activity. The first line medication for status epilepticus is: o Diazepam 10 mg PO. A patient in status epilepticus will be unable to take any medication by

mouth o Midazolam 1 mg IV. Although midazolam is used as a secondary drug in status epilepticus,

the dose would be much higher, ie, 10 mg o Phenobarbital 30 mg IV. The drug is considered a second-line drug and the dosing is 20

mg/kg IV given slowly 50–100 mg/min o Lorazepam 2 mg IV

Brain Tumors

Facts/Stats o Incidence

Primary—36,000/year Secondary—18,000/year

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o Males >females o Age: 40–60 age group o Classification

Benign: regular cell structure Malignant: infiltrates brain tissue, poor boundaries, rapid mitotic activity, necrosis Location: supra vs infratentorial Primary vs secondary Intra-axial (glial cells) vs extra-axial (meninges, CN, pituitary, and cysts) Histological origin

Intrinsic Tumors o Astrocytoma and GBM

Grade I‒IV o Oligodendrocytoma

White matter Frontal and parietal lobes

o Ependymoma Ependymal cells in ventricles

o Medulloblastoma Highly malignant in young children

Extrinsic Tumors o Meningiomas

Benign, slow growing o Neuromas

Acoustic tumor (CN VIII) Schwannoma

o Neurofibromatosis Type I: café au lait spots Type II: bilateral hearing loss

Congenital Tumors o Hemangioblastoma

Slow growing, vascular tumor Common in cerebellum

o Craniopharyngioma Embryonic Rathke’s pouch/suprasellar Arise from pituitary hypophysis

ICP, pituitary/hypothalamic dysfunction

Visual disturbances

Pituitary Tumors o Secreting

ACTH (Cushing) or GH (gigantism) o Non-secreting (90% space occupying)

Compresses pituitary: visual/hypopituitary

Pathophysiology o Increased ICP o Tumor growth o Cerebral edema

Tissue surrounding the vicinity of tumor

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Endothelial cells of white matter Increase permeability of plasma and vasogenic edema

Signs/Symptoms o Headache o Seizure o Vomiting o Alterations in consciousness o Localizing signs

Signs/Symptoms o Tumor area

Frontal: affect, motor, speech, behavior Parietal: numbness, sensory Temporal: psychomotor seizures/receptive aphasia Occipital: vision Pituitary: visual, headaches, Cushing, acromegaly Ventricles: hydrocephalus, headache, changes in LOC Cerebellum: ataxia, incoordination, dysmetria Brainstem: CN defects, vomiting, respiratory

Complications of Tumor Growth o Edema o Increased ICP o Seizures o Hydrocephalus o Hormonal changes o Focal deficits

Treatment o Stereotactic therapy o Craniotomy o Gamma knife o Conventional radiation o Brachytherapy o Chemotherapy o Gene therapy/virus therapy

Nursing Interventions o Pre-op: steroids, anticonvulsants, body image o Post-op:

ABC Monitor neurologic status Watch for seizures

Phenytoin: dosing/levels System support Family/patient support

o Pituitary tumors Watch I/O, Na+, specific gravity

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Review Questions Question #14—HH, a 45-year-old right-handed male, presents to the ED with headache, right

arm weakness with right facial droop and difficulty expressing speech. A CT scan reveals diffuse cerebral edema surrounded by a ring-enhancing lesion. The most likely location of the mass is: o Right parietal lobe of cerebral hemisphere o Left temporal lobe of cerebral hemisphere o Right frontal lobe of cerebral hemisphere o Left frontal lobe of cerebral hemisphere

Question #14 rationale—HH, a 45-year-old right-handed male, presents to the ED with headache, right arm weakness with right facial droop and difficulty expressing speech. A CT scan reveals diffuse cerebral edema surrounded by a ring-enhancing lesion. The most likely location of the mass is: o Right parietal lobe of cerebral hemisphere. The right parietal lobe’s main function is sensory

perception, body awareness, and sensory interpretation of input affecting the left side of the body

o Left temporal lobe of cerebral hemisphere. The left temporal lobe’s main function is interpretation of hearing, auditory perception, short-term memory and comprehension of the spoken word

o Right frontal lobe of cerebral hemisphere. The right frontal lobe is responsible for higher mental functions and movement to the left arm/leg/face. The right frontal lobe in right-handed individuals is considered to be the non-dominant hemisphere. Expressing speech is located in the dominant hemisphere in the frontal lobe

o Left frontal lobe of cerebral hemisphere

Question #15 —TP, a 53-year-old male, has been diagnosed with a brain mass. His symptoms include: contralateral sensory loss, neglect to the left side, and inability to draw with loss of spatial orientation. The most likely area of the brain affected is: o Parietal lobe o Frontal lobe o Temporal lobe o Occipital lobe

Question #15 rationale—TP, a 53-year-old male, has been diagnosed with a brain mass. His symptoms include: contralateral sensory loss, neglect to the left side, and inability to draw with loss of spatial orientation. The most likely area of the brain affected is: o Parietal lobe o Frontal lobe. Tumors in this area affect motor to the opposite side, speech (if dominant

hemisphere), judgment, personality, initiation, and continence o Temporal lobe. Tumors in this area present with receptive aphasia (dominant hemisphere

only) and some visual field cuts o Occipital lobe. Tumors in this area affect visual perception and field of vision

Question #16 —TP undergoes a craniotomy for debulking of a large tumor. Postoperatively, he is extubated and admitted to the ICU. After 1 hour, TP sustains a generalized seizure lasting 45 seconds. What is your initial intervention? o Check the pupillary reaction o Administer IV midazolam

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o Assess airway and breathing and prepare for possible intubation o Get a stat CT of the brain

Question #16 rationale—TP undergoes a craniotomy for debulking of a large tumor. Postoperatively, he is extubated and admitted to the ICU. After 1 hour, TP sustains a generalized seizure lasting 45 seconds. What is your initial intervention? o Check the pupillary reaction. Although the pupils need to be checked, it would not precede

assessing the airway o Administer IV midazolam. Airway stabilization is first. Lorazepam IV would be the

preferential medication of choice to reduce recurrence o Assess airway and breathing and prepare for possible intubation o Get a stat CT of the brain. This intervention would be done after the other three

interventions

Chronic Neurologic Disorders Parkinson’s Disease

o Neurodegenerative disorder caused by: Depletion of dopamine producing cells in substantia nigra Average onset is age 60, higher in men /Caucasian

o Cardinal signs o Resting tremor, rigidity, bradykinesia, and diminished postural stability

o Other Increased risk of falls Can have depression/dementia/anxiety/psychosis Other: apathy, sleep disturbances, impulse control disorders Autonomic dysfunction: urinary incontinence, sexual dysfunction, constipation,

orthostatic hypotension, impaired thermoregulation, sensory abnormalities Dysphagia/excessive drooling

Parkinson’s Treatment o Pharmacologic

L-dopa: Carbidopa plus L-dopa (Sinemet) Dopamine agonists: 1st line tx Amantadine (Symmetrel): tx dyskinesias Catechol-O-methyl transferase (COMT) inhibitors: used adjunctively to ldopa to prevent

breakdown of dopamine and prolong availability of L-dopa o Surgical interventions

Deep brain stimulation: target subthalamic nucleus or globus pallidus interna

Permits return of normal or near normal downstream outputs, allowing normalization of motor and/or limbic function

Deep brain stimulation: post op

Observe for changes in neuro exam

Keep systolic BP < 150 mm hg for first 24 hours

IV antibiotics 24-48 hours

Stool softeners / anti-embolic devices

Deep breathing/coughing to reduce pneumonia Device turned on 2-3 weeks after placed

Myasthenia Gravis

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o Description: autoimmunie disorder in which normal transmission of nerve impulses are interrupted at the neuromuscular junction. Affects voluntary muscle groups including ocular, oropharyngeal, facial, shoulders, and

arms/legs

Proximal > distal

Characterized by fluctuating and fatigable muscle weakness exacerbated by exercise and improves with rest

o Affects women > men; usually 20s and 30s o Etiology

Acquired autoimmune process related to receptors for acetylcholine at muscle surface reduced by auto-antibodies leads to impaired neuromuscular transmission and weakness.

Thymus abnormalities may be responsible for causing immune attack on the muscle receptors

o Initial manifestations:. Ptosis/diplopia 80% of cases Oropharyngeal weakness – painless/fatigable dysphagia or dysphonia Fatigable limb weakness during course of day Fluctuate over time; worsens after sustained activity Exacerbation r/t systemic illness, fever, surgery, menses, pregnancy, hypothyroidism,

heat, or stress o Signs and symptoms

Subjective

Muscle weakness

Diplopia/ptosis

Slurred speech

Dysphagia

Shortness of breath Objective

Weakness – more proximal

May have inability to lay flat – orthopnea

Frequent yawning, sighing

Difficulty swallowing o EMG o Edrophonium chloride (Bioniche test): short acting antichoinesterase inhibitor

Requires IV administration 2 mg/ test for strength 45-60 seconds later. Can repeat up to 10 mg

Positive if improvement in strength seen (effect disappears in 5 minutes) Use with caution: bradycardia/asystole, excessive salivation, bronchial secretions

o Treatment Administration of anticholiesterase inhibitors

Prevents rapid destruction of Ach

Pyridostigmine (Mestinon) must be given on time with no missed dose

Corticosteroids/immunosuppressive agents

Cyclosporine (Neoral): inhibits t-cell immune responses

Plasma exchange

IVIG: temporary intervention

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Mycophenolate mofetil (CellCept): immunosuppressive agent reduces the production of antibodies by attacking the receptor sites of neuromuscular junction

Surgical intervention: thymectomy

Nursing: administer drugs on time, patient education