CCRN/PCCN Review Neurology - FOCUS CONFERENCES · 3/17/2014 12 MG Etiology •T cells and various antibodies attack and impair or destroy acetylcholine receptors at the motor end-plate

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CCRN/PCCN Review Neurology

Cynthia Bautista, PhD, CNRN, SCRN, CCNS, ACNS-BC

Neuroscience Clinical Nurse Specialist

Yale-New Haven Hospital

[email protected]

Questions on Exam

• 12% CCRN Neurology

– 18 questions

• 5% PCCN Neurology

– 5-6 questions

– Cerebrovascular Malformation

– Encephalopathy

– Intracranial Hemorrhage

– Seizures

– Stroke Copyright Nursing Brains, LLC

Neuro Anatomy

• Cerebrum

•Frontal Lobe •Motor, personality, Brocca speech

•Temporal Lobe •Seizure, Wernicke speech, hearing

•Parietal Lobe •Sensation

•Occipital Lobe •Vision

Copyright Nursing Brains, LLC

Cerebellum and Brain Stem

• Cerebellum

– Coordination and Balance

• Brain Stem

– Cranial Nerves

– Motor/Sensory Pathways

– “RESPIRATORY”/Cardiac Center

– Reticular Activating System (alert/awake)


Neurological Assessment


Level of Consciousness Glasgow Coma Scale

• Eye Opening

– 4 - Spontaneous

– 3 - To Speech

– 2 - To Pain

– 1 – None

• Verbal Response

– 5 - Oriented

– 4 - Confused

– 3 - Inappropriate Words

– 2 - Inappropriate Sounds

– 1 - None

• Motor Response

– 6 - Obeys Commands

– 5 - Localizes

– 4 - Withdraws

– 3 - Abnormal Flexion

– 2 - Abnormal Extension

– 1 -None

“BEST INDICATOR FOR CHANGE IN NEUROLOGICAL FUNCTION”


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Cranial Nerves

CN III: Pupil reaction, ipsilateral to injury CN V, VII, IX, X, XII: Eating, prevent aspiration


Motor Response

• Motor Strength Scale

– Movement against Gravity and Resistance

• 5- Normal movement

• 4- Movement against moderate gravity and resistance

• 3- Movement against gravity only

• 2- Movement but not against gravity

• 1- Muscle contraction

• 0- No movement

“CONTRALATERAL TO INJURY”


Vital Signs

• Temperature

– Hyperthermia, hypothermia

• Pulse

– Bradycardia

• Blood Pressure

– Elevated systolic, widen pulse pressure

• Respirations

– Central Neurogenic Hyperventilation, Apneusis, Cluster breathing, Ataxic breathing, Chenyne Stokes

“CUSHINGS TRIAD – ICP LATE SIGN”


Abnormal Respiratory Patterns

Cheyne-Strokes

Central Neurogenic Hyperventilation

Apneustic

Cluster Breathing

Ataxic Breathing


Head Trauma

Mild Head Injury

• Concussion – Violent shaking of the brain

– Postconcussion Syndrome • Confusion, forgets things, loses temper,

impulsive, has a harder time learning, problems at work/school, personality change


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Contusion

• Bruising of brain tissue

• Frontal or temporal lobe

• Maximum edema occurs up to 36 hours

• Coup – Contrecoup Injury


Diffuse Axonal Injury (DAI)

• Severe mechanical disruption of neuronal pathways (shearing injury)

• Rapid acceleration and deceleration

• Immediate/prolonged unconsciousness

• MRI to diagnose

• High morbidity rate

• Vegetative care


Penetrating

• Most lethal brain injury

• 90% mortality rate

• Handgun

• Rifle

• Shotgun


Penetrating Head Injury Outcomes

• Presenting Neuro Status – Awake = survive

– Comatose = death

• Path of Bullet – Single hemisphere = survive

– Bilateral hemispheres = death

• Caliber & Velocity of Bullet – Small & slow = survive

– Large & fast = death


Penetrating Head Injury Outcomes (con’t)

• Time to Treatment

– Quick arrival to ED= survive

– Delay in arrival to ED= death

• Nature of Shooting

– Assault = survive

– Suicide = death


Basilar Skull Fracture

Anterior Fossa

•Rhinorrhea

•Anosmia

•Raccoon eyes

•Drip Pad for rhinorrhea

Middle Fossa

•Otorrhea

•Decreased hearing

•Battle signs (24-48° after injury)

•Bedrest


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Interventions

• Airway – Breathing

– Oxygenate, ventilate (PCO2 30-35)

– Suction only when necessary (2 passes)

• Circulation

– Maintain CPP > 60mmHg

– Normovolemia

• Drain CSF

• Control stimulation

– Narcotic, sedatives, barbiturates

• Regulating nursing activities

• Thermoregulation

– Normothermic (96.8° – 98.6°F, 36°-37°C)


Hydrocephalus

Hydrocephalus Pathophysiology

• Obstructive Hydrocephalus

– Obstruction of ventricular system

– Treat with ventriculostomy, treat edema

• Communicating Hydrocephalus

– Interference with reabsorption of CSF

– Treat with ventriculostomy, treat hemorrhage


Hydrocephalus Assessment & Management

• Assessment

– LOC, pupils, motor strength

• Management

– Treat the cause

– Ventriculostomy

– Lumbar drain

– VP Shunt


Intracranial Hemorrhage PCCN PAY ATTENTION!!!!

Cerebral Aneurysm

• “Worst headache of my life”

• Hunt and Hess

– Grade I- minimal headache

– Grade II- mod/severe HA, min neuro deficits

– Grade III- Drowsy, mild neuro deficits

– Grade IV- Stuporous, mild/severe hemiparesis

– Grade V- comatose, posturing

• CT Scan

• MRI

• Cerebral angiogram


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Aneurysm Management

Endovascular Procedure

•Coils

•Stents

Surgical Treatment

•Clipping


Aneurysm Management

• Prevent Rebleeding

– Decrease environmental stimuli

– Avoid valsalva

– SBP < 150 mmHg (pretreatment)

– Administer antihypertensives (Labetalol)

• Prevent Vasospasm

– SBP 160 – 180 mmHg (posttreatment)

– Calcium channel blocker (Nimodipine)

– Triple H therapy

• Hypertension, Hypervolemia, Hemodilution


SAH Complications

• Vasospasm

– Abnormal narrowing of artery

– Occurs day 3 to 2-3 weeks after rupture

– Peaks 7-14 days

• Rebleeding

– Lysis of clot or hypertension

– Occurs 24 hours or 7-10 days after rupture

• Hydrocephalus

– Due to SAH, obstructing arachnoid villi

– Place ventriculostomy, VP Shunt


Arterial Venous Malformation

• Congenital malformation

• Detected age 20 – 50 yrs

• Vessels of high pressure flow into vessels of low pressure

• Vessels rupture - headache

• Treatment

– Embolization

– Surgical removal

– Radiation


Epidural Hematoma

• Arterial bleed

– Temporal bone

– Middle meningeal artery

• Unconscious Conscious Unconscious

• Medical emergency

– Evacuation of hematoma


Subdural Hemorrhage

• Venous bleed – Acute

• Symptoms occurs < 48 hours from injury

– Subacute • Symptoms occur 48 hours to 2

weeks from injury

– Chronic • Symptoms occur > 2 weeks

from injury

• Elderly and alcoholics

• Patient on anticoagulants

– Evacuation of hematoma

– Allow to reabsorb on own


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Intracranial Hemorrhage

• Subarachnoid Hemorrhage – Severe head injury

• Intraventricular Hemorrhage – Secondary to SAH

– Extension of ICH

• Intracerebral Hemorrhage – Related to contusion

– Frontal & temporal lobes


Stroke PCCN PAY ATTENTION!!!!

Ischemic Stroke

• Accounts for 80% of strokes

• Caused by thrombosis or embolism


Signs/Symptoms F-A-S-T

– F = FACE numbness or weakness especially one side of body

– A = ARM numbness or weakness one side of body

– S = SPEECH slurred or difficulty speaking or understanding

– T = TIME to immediately call 9-1-1 and note

time symptoms started or last time person was seen normal


Ischemic Stroke Management

• Oxygenation (pulse ox >92%)

• BP Control ( 185/110)

– Antihypertensives (labetalol)

• Glucose control

• Thrombolytics (t-PA)

– Time of symptom onset (3hours), CT Scan, weight, 0.9mg/kg, bolus 10% of total dose over 1”, remaining dose over 60”

– Monitor BP and Neuro exam

• Antiplatelets (ASA, Plavix, Aggrenox)

• Anticoagulants (Coumadin)


Hemorrhagic Stroke

• Accounts for 20% of strokes

• Caused by vessel rupture

• Hypertension common cause


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Hemorrhagic Stroke Signs and Symptoms

• Severe headache

• Loss of consciousness

• Contralateral hemiparesis/hemiplegia

• Nausea, vomiting


Hemorrhagic Stroke Management

• Maintain airway

• BP Management

– Labetalol, Nicardipine

• Control ICP

– HOB 30 degrees, Hyperventilate, Mannitol


Encephalpathy PCCN PAY ATTENTION!!!!

Pathophysiology

• Neurologic degeneration

– Direct or indirect effect on brain

• Build up of toxic metabolic products

• Structural changes

• Changes in blood flow to brain

• Changes in electrical activity

• Change in supply of neurotransmitter substance

• Not a disease, results from other disease


Hypoxia/Anoxia

• Airway obstruction

• Arterial obstruction

• Cardiac arrest


Hypoxic-Ischemic

• Embolic

• Thrombotic

• Fat embolism

• DIC


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Metabolic

• Hepatic

• Renal

• Electrolyte imbalance

• Progressive symptom onset

• Coma precedes motor abnormalities

• Pupil reaction preserved


Infectious

• Menigitis

• Encephalitis

• Vasculitis


Nursing Assessment/Management

• Assessment

– Level of consciousness - decreased

– Chronic alcohol abuse

• Management

– Monitor level of consciousness

– Treat underlying condition

– Supportive care


Brain Death

• Irreversible cessation of entire brain, including brain stem

• Known cause of coma

• Absence of the following reflexes

– Nonreactive pupils (CN III)

– Doll’s eyes (oculocephalic)

– Cold calorics (oculovestibular)

– Corneal (CN V)

– Cough

– Gag (CN IX and X)

– Spontaneous respirations (Apnea Test)


Seizures PCCN PAY ATTENTION!!!!!

Partial Seizures

• 80% of people who have seizures

• Starts in only one part of the cerebral cortex - it can spread

OR

• Stars focally and spreads slowly


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• Simple Partial Seizure

– Hand may shake

– Mouth may twitch uncontrollably

– Dizzy, unusual feeling, smell, sound, or sight

– Doesn’t affect consciousness

– Lasts less than a minute


• Complex Partial Seizure

– Staring straight ahead

– Looking around

– Fidgeting with clothes

– Lip smacking

– Aimless wandering

– Automatic hand movement

– LOC is impaired

– Last 1 -2 minutes


Generalized Seizures

• 20% of people who have seizures

• Involvement of both hemispheres

• Consciousness may be impaired

• Bilateral motor manifestations


• Tonic - Clonic Seizure

– Grand Mal

– Entire cerebral cortex is involved

– Aura

– Tonic Phase

– Clonic Phase

– Doesn’t feel, see, or remember anything during seizure


• Absence Seizure

– Petit Mal

– Affects layers of the cerebral cortex associated with sensory input

– Brief loss of consciousness

– Last less than 15 seconds

– Subtle signs

– More often in children


• Myoclonic Seizure

– Generalized jerking of an extremity

– May cause patient to fall

– Less than 5 seconds

– Brief, easy to miss period of unconsciousness

– Occur in clusters


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• Atonic Seizure

– Sudden loss of muscle tone (fall)

– Loss of consciousness


Diagnostic Evaluation

• History

• EEG

• CT/MRI

• Continuous AV/EEG Monitoring

• SPECT


Management

• Protect patient from injury – Move objects, stay with patient,

padded bed rails, low bed

• Observe and record seizure activity – Note time of onset, body parts

involved, incontinence,

• Assess airway and breathing – Head-tilt, chin lift

– Oxygen, suction

– Turn patient on side (aspiration risk)

• Medication administration – Benzodiazepine

– Antiepileptic drug

– Drug levels


Neuromuscular Disorders PCCN you can leave now…..

Muscular Dystrophy

• Myopathy

– Progressive muscular weakness

• Most common hereditary myopathy

• Four common types of MD

– Duchennes (DMD)

– Becker (BMD)

– Limb-Girdle Muscular Dystrophy (LGMD)

– Facioscapulohumeral (FSHD)


Duchenne’s Muscular Dystrophy (DMD)

• Most common form of MD

• X-linked and primarily affects males

• Symptoms begin by age 5

• Death by 3rd decade


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MD Signs and Symptoms

• Toe walking and waddling gait

• Generalized hypotonia

• Weakness most pronounced in proximal lower extremities

• Gower’s sign

– Uses arms to stand and climb up body

• Pseudohypertrophy of calves

– Fatty infiltration of muscle

• Cardiomyopathy


MD Diagnostics and Treatment

• Diagnostics

– Serum CK

– Genetic testing

– NCV, EMG

– MRI with contrast

– Muscle biopsy

– EKG, echo

• Treatment

– No definitive treatment

– Prednisone

– PT, OT

– Surgical contracture release and fusion


Guillain-Barré Syndrome

• Description

– Inflammatory process of the nervous system

– Demyelination of peripheral nerves

– Preceded by suspected viral infection

– Accompanied by fever


Guillain-Barré Syndrome (con’t)

• Signs/Symptoms

– Progressive, symmetrical, ASCENDING paralysis

– Difficulty in speech, swallowing, mastication (50% of cases)

– Impairment of muscles of respiration

– ASCENDING bilateral flaccid paralysis with pain

– Autonomic dysfunction (hypotension, hypertension, ileus, arrhythmias)

– No decrease in LOC

– CSF has high protein count

– EMG slowing conduction


Guillain-Barré Syndrome (con’t)

• Management

– Supportive care (immobility & pain issues)

– Plasma exchange QOD for 10-15 days

– IVIG over 3-5 days

– Airway management

– Adequate hydration and nutrition


Myasthenia Gravis

• Chronic, progressive autoimmune-mediated disorder

• Causes sporadic weakness of the skeletal muscles

– Primarily in the face, lips, tongue, neck and throat

– Eyelid drooping and double vision

• Muscle weakness with exercise and improved muscle strength with rest

• No cure – death (40-70%) due to respiratory arrest


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MG Etiology

• T cells and various antibodies attack and impair or destroy acetylcholine receptors at the motor end-plate of neuromuscular

junction

– Decreased number of acetylcholine receptors at neuromuscular junction

• 75% abnormal thymus

• 85% hyperplasia of thymus

• 15% thymoma


MG Signs and Symptoms

Voluntary muscle weakness

Exacerbated by continuous use, warmer climates, and stress

Increased fatigue in the AM

Diplopia, weak EOMs, and ptosis

Dysphagia

Difficulty/weakness chewing

Difficulty swallowing / choking


MG Diagnostic Test

• Three tests required for diagnosis Acetylcholine receptor antibody blood test

• 85% MG patients have antibody • 50% Occular MG

Anti-MuSK antibody blood test • Test negative for above then 70% MG patients have

antibody

Tensilon (edrophonium) challenge test • Give IV 2-5mg (max 10mg) (duration 5 minutes) • Increases level of acetylcholine at junction by

blocking acetylcholinesterase • Test + if muscle strength improves • False negative reported with ocular MG

Electromyography (EMG): nerve stimulation test showing speed between stimulation and muscle contraction; slowed with MG


MG Medications

• Acetylcholinesterase inhibitors Allows ACTH to remain in neuromuscular

junction longer

Pyridostigmine (Mestinon) • 60mg every 4 hours • Time released every 12 hours

Neostigmine (Prostigmin) • 2 hour duration

– Take prior to activity, assess motor strength and secretions

– Give medications on time, within 30” of food, and with snack (GI upset)

– Atropine to tx diarrhea/salivation from acetylcholinesterase inhibitors

– Decrease dose for fasiculations due to nicotinic effects


MG Medications

• Immunosuppressants Prednisone

• 20-60mg/day

• Give potassium chloride, calcium carbonate, vitamin D 2 to side effects

Azathioprine (Imuran) • 2-3mg/kg/day, divided doses (usually 50mg

TID)

• Takes up to 6 months for effect

Cyclophosphamide (Cytoxan) – rarely used due to toxicity

• Reboot immune system

• 1.5 - 5mg/kg/day

• Usually 100-200mg a day


MG Treatment

• Plasmaphoresis and plasma exchange – Removes antibodies

– Short term treatment– must be done regularly

– Especially useful for crisis treatment

• Intravenous immunoglobulin (IVIG) – Pooled human gamma globulin

– Short term treatment of serious relapse

– Begin 1 – 2 weeks of onset

– 2g/kg dose over 2-5 days

– Improvement in 4-5 days, lasts about 1 month


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MG Crisis

• Respiratory support is essential in both crisis

• Myasthenic is due to infection

• Cholinergic is due to over medication


Neurologic Infectious Diseases

Meningitis

• Description

– Inflammation of meninges

• Infective agent

– Bacterial: streptococcus pneumonia, neisseria meningitidis, H. influenzae, direct, hematogenous, CSF leak entry

– Viral: enteroviruses, arboviruses, herpes viruses, fecal-oral contamination, respiratory droplets

– Fungal: cryptococcus neoformans, open wound, mucous membrane


Meningitis • Signs/Symptoms

– Headache, fever, nausea, vomiting

– Nuchal rigidity, Kernig’s, Brudinski's, photophobia

– Altered LOC, seizures

– CSF

• Bacterial: Cloudy, protein, glucose

• Viral: Clear, protein, normal glucose

• Management

– Control symptoms

– Antibiotics, antiviral, antifungal

– Assess LOC

– Assess for ICP

– Monitor temperature


West Nile Virus

• Arbovirus—mosquito-borne viruses that are transmitted by blood-feeding arthropods

• Transmission

– Blood transfusion

– Organ transplantation

– Breast milk

– Intrauterine

– Laboratory acquisition

• Incubation period of 3–14 days


West Nile Virus

• Clinical presentation of mild Infection

• 20% of people develop mild infection

• Flu-like symptoms: Fever,

headache, nausea and vomiting, backache, malaise, myalgia, maculopapular rash

• Symptoms may last 3–6 days


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West Nile Virus

• Personal protective

– Avoid being outdoors at dawn and dusk

– Wear light-colored, long clothing

– Use DEET insect repellent

– Drain standing water


Lyme Disease

• Ticks transmit Lyme borreliosis during a blood meal

• Occurs May–Sept.

• Tick must be attached for 24–72 hrs

• Serology studies

– ELISA a positive IgM response

– Western blot used as confirmatory test if ELISA is positive


Lyme Stage 1: Early Localized

• Skin lesions: erythema migrans at site of tick bite (60–80%)

– A “bull’s eye”—a target center, expanding central area and an outer border

• Flu-like symptoms

– Headache, malaise, fatigue, or myalgias


Lyme Stage 2: Early Disseminated

• Acute neuroborreliosis appears weeks, months

• Malaise, fatigue, lymphadenopathy

• Nervous System:

– Meningeal signs, headache, neck stiffness, difficult concentrating, cranial nerve dysfunction, Bell’s palsy, radiculopathies, and ataxia

• Cardiac System:

– Atrioventricular block, myopericarditis, pancarditis

• Lyme arthritis


Lyme Stage 3: Late Chronic

• Nervous system and joints continuous inflammation for >1 year

• Cognitive changes and fatigue

• Lyme encephalopathy,

polyneuropathy, and leukoencephalitis

• Chronic arthritis

• Lymphocytoma; acrodermatitis, chronica atrophicans


Lyme Disease - Management

• Early infection

– 10–21 days antibiotics

• Doxycycline for adults and children >8 years

• Amoxicillin for children < 8 years

• Late infection

– Ceftriaxone given IV for 2–4 weeks

– Cefotaxime or penicillin G (alternative)


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Lyme Prevention

• Check for ticks after being outdoors

• Wear light clothing, long sleeves, and pants

• Apply tick/insect repellent to clothing

• Remove tick properly: grasp tick with tweezers or a piece of tissue, then pull straight out

• Human vaccine: available

– Booster injections needed every 1–3 years

• Vaccinate pets annually and check for ticks


Bell’s Palsy

• Herpes virus causes inflammation/compression of CN VII (Facial Nerve)

• Unilateral facial weakness

• Steroids and antiviral agents

– Prednisone and acyclovir


Brain Tumor

• Primary—unknown

• Metastatic

– 35% lung

– 20% breast

– 10% kidney

– 10% gastrointestinal tract

Brain Tumor Etiology


• Gliomas – low-grade glioma – astrocytoma – anaplastic astrocytoma – glioblastoma multiforme

• Ependymomas

• Medulloblastoma

• CNS Lymphoma

Intra-axial Brain Tumors


Extra-axial Brain Tumor

• Menigioma

• Metastatic

• Acoustic Neuroma (Schawonoma)

– CN VIII

• Pituitary adenoma

• Neurofibroma (neurofibromatosis)

– Peripheral nerve

– Genetic, autosomal dominate


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Brain Tumor Surgical Treatment

• Biopsy

• Craniotomy

• Stereotaxis Surgery

• Transsphenoidal/Endoscopic


Brain Tumor Radiation Therapy

• Damages DNA of rapidly dividing cells

• 4000–6000 cGy total dose

• Duration of 4–8 weeks

• Side Effects – Skin burns, hair loss, fatigue,

local swelling

• Patient teaching includes “do not erase” markings

• Radiation necrosis


Brain Tumor Chemotherapy

• Slows cell growth

• Cytotoxic Drugs – CCNU, BCNU, PCV, Cisplatin,

Etoposide, Vincristine, Temozolomide (Temodar)

• Side effects – Oral mucositis, bone marrow

suppression, fatigue, hair loss, nausea and vomiting, anxiety, peripheral neuropathy


Neurosurgery

Postop Neurological Deficits

• Diminished level of consciousness

• Communication deficits – Expressive/receptive aphasia

(cerebral edema)

• Motor and sensory deficits

• Headache – First few days

– Check head dressing

– Codeine, Tylenol #3



• Elevated temperature

– Hypothalamus, infection

– Antipyretics, hypothermia blanket

• Periocular edema

– Discoloration, ecchymosis

– Peak 48 – 72 hours (edema last 5 days, ecchymosis last 12 days)

– Cold compress

• Diminished gag/swallow (CN IX & X)

– Posterior fossa surgery


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• Visual disturbances

– Diplopia (eye patch)

– Field cuts (scan the room)

• Loss of corneal reflex

– Eye shield, tape lid shut, artificial tears

• Personality changes

– Edema, drugs, stress, surgery


Nursing Management

• Incision

– Skin flap

– Sutures/stapes removed 7-10 days

• Supratentorial

• Infratentorial


Nursing Management

• Head Dressing

– Turban style dressing

– MD to remove after 24 hours

– Monitor for blood or CSF

– Once removed observe incision for redness, drainage, or signs of wound infection


Nursing Management

• Positioning Head of Bed – Elevate HOB 30 degrees

– Maintain neck in neutral position

• Turning and Positioning – No restriction

• Ambulation – Allowed OOB as soon as tolerated

– Infratentorial caution with dizziness


Nursing Management

• Fluid and Electrolyte Balance – Maintain euvolemia

– Record I & O

– Monitor electrolyte and osmolarity

• DVT Prophylaxis – Sequential compression device

– Heparin, Lovenox

• Administer analgesics as ordered


Postoperative Complications

• Cerebral hemorrhage

• Increased intracranial pressure – Peak 72 hours

• Tension pneumocephalus – Entry of air, posterior fossa craniotomy

– Within 24 hours to 1 week

• Hydrocephalus – Edema or subarachnoid bleeding


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Postoperative Complications

• Seizures

– Within first 7 days, focal seizure

– Prophylactic anticonvulsants

• CSF Leakage

• Meningitis

– Prophylactic antibiotics

• Wound infection

– Staphylococcal

– Redness, drainage, foul odor, elevated WBC


Documents

CCRN/PCCN Review Neurology - FOCUS CONFERENCES · 3/17/2014 12 MG Etiology •T cells and various antibodies attack and impair or destroy acetylcholine receptors at the motor end-plate