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NEUROLOGIC
EMERGENCIES
Nina Bates, BSN, RN
Revised by
Elena Stock, BSN, RN
Reference: Sheehy’s Manual of Emergency Care, 7th Edition
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Neurologic Assessment in the ED
• Level of Consciousness
• Most reliable indicator of change in patient’s neuro status
• 2 components:
• Arousal (responsiveness)
• AVPU
• Awareness
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Glasgow Coma Scale
Three components:
• Eye opening
• Verbal Response
• Best Motor Response
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Glasgow Coma Scale
Eye opening
• 4: Spontaneous: eyes open without stimulation
• 3: To verbal (not necessarily to command)
• 2: To pain
• 1: None
Verbal Response
• 5: Oriented x4
• 4: Confused, but use of language is correct
• 3: Inappropriate words
• 2: Incomprehensible words
• 1: None- no words/sounds despite stimulation
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Glasgow Coma Scale
Best Motor Response
• 6: Obeys commands
• 5: Localizes to pain
• 4: Withdraws from pain
• 3: Abnormal Flexion
• 2: Extension
• 1: Flaccid
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Glasgow Coma Scale
• 15-13: Normal- mildly altered
• 12-9: Moderate abnormality
• 8 or Less: Severely altered (comatose)
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AEIOU-TIPS for AMS
• A: Alcohol
• E: Epilepsy (seizure), environmental
• I: Insulin (too much, too little)
• O: Oxygen (hypoxia, hyperoxia)
• U: Uremia (metabolic disorders)
• T: Trauma, toxicity, tumor
• I: Infection, ischemia
• P: Psych, poisoning
• S: Stroke, syncope
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SELECTED EMERGENCIES
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COMA
• Prolonged state of unconsciousness
• Swift action to preserve life and brain function
• Initial work up is critical to establish correct diagnosis and treatment
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Common Causes of Coma in the ER
• Trauma (primary or secondary)
• Cerebrovascular disease (hemorrhagic or ischemic stroke, dissection)
• Intoxications (ETOH, recreational drugs, medications, environmental toxins, CO2)
• Infections (bacterial, viral, fungal)
• Metabolic derangements
• Postictal state
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Initial Interventions
• Evaluate A, B, C’s and c-spine (if concerned for trauma)
• Assess LOC (AVPU)
• IV access
• Meds:
• Glucose, BG <70, give D50
• Thiamine 100 mg IV (prevent Wernicke’s
encephalopathy)
• Narcan IV
• Fluids
• Labs
• Radiology
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Details Are Important
• Time course of unconsciousness
• Abrupt vs. gradual onset
• Medications
• Toxin exposure
• Social history
• Past medical/surgical history
• Neurological exam findings
• Abnormal labs
• Results of Head CT, LP or EEG if available
• Response to treatments given
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CAUSES OF COMA
STRUCTURAL
FOCAL EXAM
• Asymmetric pupillary
abnormalities
• Unilateral weakness, paralysis
• Aphasia, dysarthria
CAUSES
• Stroke, trauma, tumor
NONSTRUCTURAL
NON FOCAL EXAM
• Progressive, gradual onset
• Symmetric cranial nerve findings
CAUSES
Medication overdose, ETOH, illicit
drug use, toxin exposure, CNS
infections, Metabolic
encephalopathy
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Key Elements for Handoff
• History of Present Illness
• Clinical presentation/Neurological exam
• Relevant PMH/PSH
• Brain imaging results
• Treatment given thus far
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Case Study #1
• A 42 year old female presents to the emergency via
squad, after being found unresponsive by her daughter.
Last known well 2200 the night.
• On initial assessment GCS is 9, and she appears be
protecting her airway. Her pupils are 4mm PERRL, but
has a right gaze deviation. She will open her eyes to
sternal rub for a few seconds, moans and mumbles some
words . She does not follow commands, and moves
extremities spontaneously, except her RUE is noted to be
weaker. A stroke alert was called at this time.
1. What immediate interventions?
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Case Study #1
• VS: HR 86, RR 18, BP 149/86, Temp 100.1, Spo2 98% on room air
• Non contrast head CT: no acute pathologies
• CTA: no large vessel occlusion
• CT perfusion: no perfusion deficit
• ABG PH 7.25, PCO2 28, HCO3 19, sats 97%
• Labs: Lactate 4.5. CBC, and Chem7 unremarkable
• Past medical history provided by daughter: • Stroke 2011
• Alcohol abuse
• Anxiety- takes xanax tid every day
• There are many possible causes of this patient being obtunded.
• Presented: RUE weakness, right gaze deviation, and elevated lactate.
• 1. What are your thoughts?
• 2. What further work up interventions?
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Courtney Kresge ACNP-BC,CCRN
• Huff, S.J.,Stevens, R.D., Weingart, S.D.,(2012). Emergency Neurological
Life Support: Approach to the Patient with Coma. Neurocritical Care Society,
DOI 10.1007/ s12028-012-9755-4 2012
• Varelas, P. N., Graffagino, C., (2013), Metabolic Encephalopathies and
Delirium. Neurocritical Care Society Practice Update. Retrieved from
www.neurocriticalcare.org/sites/.../ 22.MetabolicEncephalopathies.final
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MENINGITIS/ ENCEPHALITIS
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Bacterial Meningitis and Viral Encephalitis
• Severity of clinical signs and symptoms may predict
prognosis
• Early interventions for maintaining airway, hemodynamic
instability, and early initiation of anti-infective is critical
• Pathogens
• Bacteria- *Emergency
• Viruses- *HSV encephalitis
• Fungi
• Parasites
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Facts
• Annual incident of
bacterial meningitis
• 4-6 cases per 100,000
• Encephalitis is less
common than
meningitis
• Literature suggest 48%
of patients will present
within the first 24 hours
of onset of symptoms
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Signs and Symptoms
• Encephalitis
• Focal neurological findings/Cortical disturbances
• New seizure onset
• Extremity weakness
• Aphasia
• Meningitis
• 44% of patients presented with classic triad
• Fever
• Stiff neck
• Mental status changes
• 95% of patients had diagnosis if two of classic triad is
present with headache
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Physical Exam
A positive sign is when clinician extends the knee from a flexed 90
degree and produces pain posterior thigh, or lower back
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Physical Exam
A positive sign is when patient is supine and the neck is passively
flexed and triggers a flexion of hips and knees
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Other Causes of Fever and Headache
• Viral infections without meningitis
• Cerebral abscess
• Severe sepsis
• Sinusitis, tooth abscess, tonsillitis
• Non-infectious conditions: SAH, cerebral venous
thrombosis, pontine hemorrhage
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BACTERIAL
• More severe, can lead to
serious complications
• Transmitted via respiratory
droplets and secretions
VIRAL (aseptic)
• Usually mild, self limited
• Not usually contagious
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Initial Assessment
• Airway, breathing and circulation evaluated immediately
• Vital signs
• Temperature >100.4F or <96.8F
• Blood pressure
• Heart rate
• Respiratory rate
• Oxygen saturation
• Glasgow Coma Scale
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Initial Interventions
• History, examination
• IV access-minimum of two 18 gauges
• POC Glucose and INR, CBC, chemistries, blood cx,
lactate
• IV resuscitation to treat shock
• If bacterial meningitis is presumed, immediate
administration of dexamethasone followed by empiric
antibiotic coverage
• Expedite transfer for Head CT
• Prep for LP after CT is reviewed
• If suspected meningococcus, exposure prophylaxis
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CT Prior To LP
• CT will be needed prior if:
• Patients with clinical presentation suggesting
meningitis/encephalitis
• Enough uncertainty of intracranial process
• If show mass/lesion that explains condition/symptoms
• Abort LP
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Antibiotic Coverage
• Should be given immediately according to sepsis
guidelines
• After obtaining blood cultures
• Do not wait for LP or CT
• Each hour of delay in the septic patient, mortality is
increased.
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Antibiotic Coverage
Community acquired
• Haemophilus influenzae, Neisseria meningitidis,
and Streptococcus pneumoniae
• Rocephin
• Vancomycin
• Acyclovir
• Ampicillin- Listeria monocytogenes
Age >55, Immuncompromised, Alcoholics
• Healthcare or Hospital acquired- ECF, HD, recent hospitalizations
MRSA and Pseudomonis
• Vancomycin
• Cefepime
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Antibiotic Prophylaxis
• Recommended for close contacts of a patient with invasive
meningococcal disease to prevent secondary cases.
• Should be initiated within 24 hours after the index patient is identified
• Prophylaxis given >2 weeks after exposure has little value
• Antibiotic regimens for prophylaxis include:
• Rifampin 600mg orally twice daily for two days
• Ciprofloxacin 500mg orally as a single dose
• Ceftriaxone 250mg as a single intra-muscular injection
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Normal Lumbar Puncture Results
• Opening pressure <20 cm H2O
• <5 WBC cells/mm3
• NO RBC
• NO xanthochromia (from the Greek xanthos = yellow)
• Protein <50 mg/dl
• CSF glucose >2/3 serum glucose
• Gram stain negative
• LP -> Normal -> Evaluate other infectious sourse
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Abnormal LP Results
Very High CSF White Cells
• Bacterial Meningitis
• WBC 100-1000
• RBC normal
• Protein High
• Glucose Low
• Gram stain (+)
Elevated WBC and NO RBC
• Viral Meningitis
• WBC 10-100
• NO RBC
• Protein normal
• Glucose normal
• Gram stain (-)
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Abnormal LP Results
Elevated WBC and RBC
• Herpes Encephalitis
• WBC 100s
• RBC 10-100 or High
• Protein normal or
elevated
• Glucose normal
• Gram stain (-)
Elevated RBC or Xanthochromia
• SAH
• WBC normal
• RBC High
• Xanthochromia
• Protein normal to elevated
• Glucose normal
• Gram stain (-)
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Case Study #2
• 26 year old female presents to the emergency department via squad after having a witnessed seizure. She is lethargic but arouses to verbal stimuli, and complaining of a 10/10 headache. There is no one present to give a detailed history
• Vital signs: BP 96/62, RR 28, Temp 101F, and Spo2 98% on room air. On exam she has no nuchal rigidity, negative Kernig’s, and Brudzinski sign. Remaining exam unremarkable
• Labs: WBC 16K, NA 130, create 0.9, BUN 10. POC glucose 80 and INR 1.2. Remaining labs were unremarkable.
• What is her possible diagnoses?
• Does she need a head CT prior to an LP?
• Do you think it is appropriate to start antibiotics at this time?
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Case Study #2
• Head CT results do not show any lesions or evidence of increased
ICP. LP was performed with the following CSF cell count.
• Elevated opening pressure
• WBC- 1,200 cells 60 % neutrophils
• Protein -70 mg/dL
• Glucose- 35 mg/dL
• Sent for Gram Stain and culture
• 1. What is this patient’s likely diagnosis?
• 2. List some nursing interventions you would want to execute within
the first hour.
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STATUS EPILEPTICUS
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SE is a Medical Emergency
• Life threatening medical and neurological
emergency
• The more prolonged the status, the more
intractable it is to treatment
• The more prolonged the status, the poorer the
prognosis for recovery
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Definition of Status Epilepticus
• > 5 minutes of continuous clinical and/or electrographic seizure activity OR recurrent seizure activity without recovery between seizures
• Convulsive SE with rhythmic jerking of extremities
• Non-convulsive SE with seizure activity seen on EEG but no clinical findings of seizure observed
• Refractory SE is that which does not respond to standard treatment regimens with adequate initial dose benzodiazepine and one antiepileptic drug
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Scope of the Problem
• 1st described in 7th century BC
• Effective management remains challenging
• ~ 1 million seizure related ER visits per year • 20% of ED visits for neurological problems
• 200,000 US patients/year status epilepticus
• 30 day mortality of generalized convulsive SE is 19-27%
• Prolonged seizures associated with higher mortality and worse clinical outcomes
Claasen et al. 2015. Neurocritical Care. ENLS SE
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Non-convulsive Status Epilepticus
• 8-20% of critically ill patients
• NCC: 18-34% of patients with cEEG monitoring have non-convulsive seizures (NCS) and 10% have non-convulsive status epilepticus (NCSE)
• Medical and surgical ICUs: 8-10% of patients with cEEG monitoring have NCSE
• Up to 48% of comatose patients after convulsive SE have NCS or NCSE
• ~ 20% of patients go from convulsive SE to NCSE after initial treatment
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Causes of Status Epilepticus
• Acute
• Metabolic dysfunction
• Infections
• CNS infections
• Stroke
• Head trauma
• Drug toxicity or
withdrawal
• Noncompliance with
AEDs
• Hypoxia
• Cardiac arrest
• Chronic
• Pre-existing epilepsy
• AED withdrawal
• Chronic alcohol abuse
• CNS tumor
• Remote CNS
pathology
• Organ failure
• Illicit drug use
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Status Epilepticus by Etiology
Cook et al NCC 2012
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Pediatric Causes of SE
• # 1 is systemic infection
• Congenital anomalies
• Anoxia
• Metabolic problems
• Antiepileptic drug withdrawal
• CNS infection
• Trauma
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Drugs that Lower the Seizure Threshold
• Theophylline (bronchodilator)
• Carbapenems (ATB)
• Fluoroquinolones (Cipro,
Levaquin)
• Isoniazid (TB ATB)
• Antidepressants (Bupropion,
TCAs)
• Accumulation of drugs with renal failure
• Metronidazole
• Meperidine (Demerol)
• Tramadol
• Lithium
• Clozapine (antipsychotic)
• Cyclosporine (immunosuppressive)
• Sympathomimetic (Neo,
Levo, Dopamine)
• Organophosphate (base of
many insecticides0
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Electrolyte Abnormalities and Seizure
• Hyponatremia
• Risk of cerebral edema and herniation
• Increased CNS neuronal irritability
• Hypocalcemia
• Increased neuromuscular excitability and tetany
• CNS neuronal irritability
• Hypomagnesemia
• Magnesium stabilizes neuronal membranes
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Phases of SE • Phase I
• First 30 minutes
• Convulsive tonic clonic seizure
• Increased autonomic activity
• Hypertension, hyperglycemia, hyperpyrexia
• Increased sweat and salivation
• Phase II
• Minor twitching, loss of clinical exam
• Decreased cerebral autoregulation
• Decreased cerebral blood flow
• Increased ICP
• Systemic hypotension
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Abou-Khalil. 2013. Vanderbilt
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Complications of SE
• Hyperthermia
• Lactic acidosis
• Rhabdomyolysis
• Acute kidney injury
• Neurogenic pulmonary
edema
• Hyperkalemia
• Arrhythmias
• Aspiration
• Impaired ventilation
• Hypertension
• Hypotension
• Hyper/hypoglycemia
• Intracranial
hypertension
• Altered cerebral
perfusion
• Permanent
neurological damage
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Diagnosis
• Diagnostics should not
delay control of
seizures
• H & P
• O2 sat
• Vital signs including
temp
• Blood glucose
• CBC
• Chemistry panel,
magnesium, calcium
• ABG
• Lactic acid
• CPK
• Toxicology screen
• AED levels
• Neuroimaging
• Lumbar puncture in
febrile patients
• EEG
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History
• Seizure description and course
• Onset and duration
• Observed signs
• Tonic clonic movements, gaze deviation, automatisms,
impaired consciousness
• Autonomic signs: HTN, tachycardia, pupillary dilation
• Past medical history
• History of prior seizure disorder
• Medication history
• AEDs and compliance
• New medications
• Social history
• Illicit drug or ETOH use or withdrawal
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Physical Exam
• LOC
• Cranial nerves
• Motor skills
• Reflexes
• Sensory exam
• Cerebellar exams
• Mental status
• Focal exam findings
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EEG
• 24 hour EEG is gold standard
• 30 minute spot EEG misses ~ 2/3 non-convulsive seizures and ½
clinical seizures
• 24 hour EEG detects 95% seizures in non-comatose and 80% in
comatose patients
• Video EEG to distinguish EEG abnormality from artifact
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Indications for EEG with SE
• Recent clinical seizure or SE without return to baseline >
10 minutes
• Coma, including post cardiac arrest
• Epileptiform activity or periodic discharges on initial 30
minute EEG
• Intracranial hemorrhage including TBI, SAH, ICH
• Duration of cEEG for minimum of 48 hours for suspected
non-convulsive seizures in patients with altered mental
status
Brophy et al NCC 2012
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Differential Diagnosis
• Status epilepticus or non-convulsive status epilepticus
• Post-ictal state
• Movement disorder
• Herniation
• Limb-shaking TIA
• Psychiatric disorder
• Toxic metabolic disorders
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Psychogenic Non-Epileptic Seizure
• “Pseudo seizure” or “Conversion Disorder”
• Non-epileptic spell simulating SE
• Not intentionally produced or feigned
• Conversion of emotional pain to physical symptoms
• Differs from malingering or factitious disorders
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Peters. Vanderbilt
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Goals of Treatment
• Airway protection and supportive care
• Rapid termination of seizure activity
• Prevention of seizure recurrence
• Manage precipitating cause(s)
• Manage complications
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Response to Treatment
• If treatment of GCSE initiates within 30 minutes of seizure
onset, 80% respond to 1st AED given
• When treatment initiates 2 hours or more after seizure
onset, 40% respond to 1st AED given
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Benzodiazepines-1st Line Therapy
• Lorazepam (Ativan) preferred benzodiazepine
• Duration of action 4-14 hours
• Higher initial response rate
• 4 mg IV, may repeat in 5-10 minutes
• Diazepam (Valium) duration of action 20 minutes
• 0.15 mg/kg IV to max of 10 mg/dose, may repeat every 5 minutes
• May give rectally
• Midazolam (Versed)
• May be given IV, IM, nasally, or buccally
• 0.2 mg/kg IM to max of 10 mg dose
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2nd Line Therapy
• Phenytoin (Dilantin)/Fosphenytoin (Cerebyx)
• 20 mg PE/kg IV (or IM), may give additional 5 mg/kg
• Complicated by hypotension and cardiac conduction disturbances
• Infuse 50 mg/min
• Valproic Acid (Depacote)
• 20-40 mg/kg IV, may give additional 20 mg/kg
• Phenobarbital: 20 mg/kg IV, may give additional 5-10
mg/kg
• Levetiracetam: 1000-3000 mg IV
• Lacosamide: 200-400 mg IV
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Treatment for Refractory SE
• Intubate
• Midazolam (Versed) infusion 0.2 mg/kg IV. Repeat 0.2-0.4 mg/kg boluses Q 5 minutes until seizure stopped. Maintenance 0.05-2.0 mg/kg/hr
• Propofol infusion 20 mcg/kg/min, titrate up to 200 mcg/kg/min.
• Pentobarbital infusion • Load 5 mg/kg IV up to 50 mg/min
• Repeat 5 mg/kg boluses until seizure stops
• Maintenance 0.5 – 10 mg/kg/hr
• Ketamine
• Therapeutic hypothermia • Seizure control and neuroprotective
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Super-Refractory SE
• Seizures resistant to 3rd line therapy
• Generally poor outcome
• Control seizures with pentobarbital infusion
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Initial Pre-hospital Therapy
• Early intervention most effective
• Benzodiazepines
• Airway adjuncts and O2
• IV or IO access
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ED 0-5 Minutes
• Obtain VS including temperature
• Ensure open airway—administer O2 if needed
• Establish IV access
• Assess for cardio-respiratory compromise
• Brief exam to observe seizure activity and focal
neurological signs
• Fingerstick glucose
• Examine for evidence of head trauma
• Draw baseline bloodwork and toxicology screen
• 1st dose benzodiazepine, repeat in 5-10 min if seizures
continue
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ED 10-45 Minutes • Additional dose lorazepam
• Loading dose AED
• Monitor EKG, pulse, BP, respiratory status while infusing drugs
• Evaluate respiratory status • Consider intubation if compromised airway or gas
exchange or suspected intracranial HTN
• Administer dextrose if hypoglycemic
• Volume resuscitation and/or vasopressor support if indicated
• Foley catheter
• Consider EEG
• Consider neuroimaging
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Initial Hospital Therapy
• Continue ABCs
• Optimize blood glucose
• Continue benzodiazepines until seizure controlled
• If not controlled, add 2nd line agent
Manno. Neurohospitalist. 2011.
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Outcomes Convulsive SE
• Mortality of CSE
• At hospital discharge 9 – 21 %
• At 30 days 19 - 27 %
• Morbidity of CSE
• Severe neuro or cognitive sequelae 11 – 16 %
• Deterioration in functional status 23 – 26 %
• Factors associated with worse outcomes
• Underlying etiology, development of SE in hospitalized patient,
older age, impaired consciousness, duration of SE, at onset focal
signs, medical complications, insufficient therapy
• Mortality rate for pediatric patients 3 - 11 %
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Outcomes of NCSE and RSE
• Mortality in NCSE
• At hospital discharge 18 – 52 %
• At 30 days 65 %
• Mortality in RSE
• At hospital discharge 23 – 61 %
• At 3 months 39 %
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References
• Brophy et al. 2012. Guidelines for the evaluation and
management of status epilepticus. Neurocritical Care Journal
17: 3-23.
• Brophy. 2015. Management of status epilepticus: Breaking
bad. Pharmacotherapy of Neurocritical Care Webcast series.
http://www.neurocriticalcare.org/news/new-release-
pharmacotherapy-neurocritical-care-series-pons-presentation
• Claassen et al. 2015. Emergency neurological life support:
Status epilepticus. Neurocritical Care Journal. Published
online.
• Laccheo et al. 2015. Non-convulsive status epilepticus and
non-convulsive seizures in neurological ICU patients.
Neurocritical Care Journal 22: 202-211.
Kay Goodall CNP
Neurocritical Care Service
Riverside Methodist Hospital
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NEUROMUSCULAR EMERGENCIES
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Neuromuscular Diseases
• Myasthenia Gravis
• Guillain-Barre syndrome
• Tetanus
• Envenomation –Snakes (Northern Copperhead,
Eastern Massasauga Rattlesnake, and the Eastern
Timber Rattlesnake), Spider ( Brown Recluse and
Black widow), Scorpions (rare but can be found in
Ohio), Sharks (Just seeing if you’re still listening).
• Organophosphorus poisoning – Insecticides,
herbicides, and Sarin gas
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Case Study
• A patient presents to the emergency department after
having diarrhea, fever and body aches that lasted for two
weeks. He states, “I think I have a flu”. Current symptoms
include tingling in both hands and weakness in his legs.
Based on the medical history and current symptoms,
which of neurological disorder is he likely to be diagnosed
with?
• A. Myasthenia Gravis
• B. Guillain-Barre syndrome
• C. Multiple Sclerosis
• D. Parkinson's Disease
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Case Study
• The correct answer is B • Rationale: Guillain-Barre syndrome (GBS), myasthenia gravis, and multiple
sclerosis are all autoimmune disorders. GBS occurs following viral or
bacterial illness, such as influenza, mononucleosis, or pneumonia. Clinical
manifestations include numbness and tingling in the hands and feet, along
with weakness in the lower extremities that ay quickly progress to paralysis
during acute phase.
• Myasthenia gravis symptoms include muscle weakness, spurred speech and
ptosis (ocular weakness) often triggered by emotional stress, menstruation,
bright sunlight, viral infection, and medications such as Cipro, beta-blockers,
and statins.
• Symptoms of multiple sclerosis include muscle cramping, bowel, bladder and
sexual dysfunction, ataxia, and tremors which manifest months or years
apart.
• Signs and symptoms of Parkinson disease include having resting tremor, gait
difficulty, reduction of sense of swell and forgetfulness.
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Recognition and Triage
• What is the differential? Life threatening to trivial
• Is it non-traumatic, spinal cord, brain, infection,
psych?
• Do I need to resuscitate or pontificate?
• Start with the basics; A,B,C,D
• Airway compromise can be from weakness of
oropharyngeal muscles or the diaphragm.
• Be vigilant when assessing for facial droop, trouble
swallowing, weak cough, or poor ventilatory effort
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Why is Neuromuscular Disease a
Concern?
• What are you assessing in your patient?
•Airway… And then?
•Breathing… And then?
•Circulation… And then?
•Disability
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Respiratory Failure
• Are there secretions, facial drooping, or dysphasia?
• Can your patient talk to you without getting short of
breath?
• Are they breathing fast and shallow using accessory
muscles?
• Are they SOB while supine, does it get better when they
stand?
• Hallmark sign not to miss! The diaphragm and respiratory muscles
may be too weak to over come the weight of the chest wall, neck,
and abdominal contents.
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Respiratory Failure - Testing
• Can they count to 20 in one breath?
• What is the resting respiratory rate?
• On going testing would include a Force Vital Capacity
(FVC), Negative inspiratory force (NIF) or Maximum
Expiratory Pressure (MEP)
• Pulse oximetry and ABGs - Although they are good tests
they show late signs of changing status.
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Treatment
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Myasthenia Gravis
• “Chronic auto immune disease mediated by acetylcholine
receptor(Ach) antibodies that act at the neuromuscular
junction.” (McCance, Huether, Brashers, Rote, 2010, pg.
639)
• Usually insidious onset.
• Fatigue following exertion, resolves with rest but reoccurs
with exertion. Due to the destruction of receptor sites for
the ACh on the postsynaptic membrane.
• The eventual destruction of the receptor sites cause nerve
transmission to be decreased.
• Cause is unknown.
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Myasthenia Gravis
• Occurs around 20 to 30 years of age
• More frequently in females
• May have a familial connection
• Many commonly prescribed drugs (antibiotics,
psychotropic and antidysrhythmic drugs) can precipitate
an event
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Clinical Manifestations
• Eyelid drooping, extra-ocular muscles weak, flaccid facial muscles, diplopia
• “Nasal speech with impaired bulbar reflexes (tongue, pharynx, larynx).
• Neck and proximal limb weakness.”
• Flower, Wainwright, Caulfield, (2015).
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Testing
• CT scan r/o thymoma
• Electromyogram (EMG)
• Acetycholine receptor antibody testing, muscle specific
tyrosine kinase (MuSK)
• Edrophonium testing (Tensilon test) – prevents break
down of acetylcholine reducing muscle weakness. Edrophonium
2 mg + Edrophonium 8 mg IV. => increased muscle srenth with MG. Administer atropine if symptoms not improved
(cholinergic chrisis)
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Treatment • Pyridostigmine or Neostigmine (for symptom relief not for
acute phase necessarily)
• Close observation in ICU
• NIFs (negative inspiratory force) and FVC (forced expiratory volume) frequently measured
• IVIG and/or Plasmapheresis (PLEX)
• Thymectomy if warranted
• Avoid anticholinesterase and aminoglycoside medication
• Steroids can be used at a low dose with long term goals of immunosuppression but not for acute phase.
• Caution with antiarrhythmic, neuromuscular blocking agents, certain antibiotics (aminoglycosides), thyroid hormones, and phenytoin to name a few.
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Myasthenia Crisis
• Respiratory failure in the setting of MG 2/2 respiratory
muscle weakness and oropharyngeal weakness
• Life threatening, rapid decompensation due to the
pathophysiology of the disease.
• May be preceded by infection (caution with antibiotics as
C-diff can be devastating), pregnancy, medication
changes including anticholinesterase and prednisone.
• Can last two weeks.
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Guillain – Barre syndrome
• Acquired acute inflammatory demyelinating or axonal polyneuropathy with four subtypes: • Acute inflammatory demyelinating polyneuropathy (AIDP)-
ascending paralysis with typically distant start, early sensory symptoms and loss of deep tendon reflexes (DTRs)
• Acute motor axonal neuropathy (AMAN) – acute progressive weakness with no sensory impairment
• Acute motor and sensory axonal neuropathy (AMSAN) – ascending paralysis
• Fisher syndrome (FS) –ophthalmoparesis, areflexia, and ataxia
• Muscles innervated by the damaged nerves may atrophy and experience denervation. If the cell body survives it may regenerate peripheral nerve and recover. If the cell body does not survive then no regeneration is possible and may lead to permanent damage.
• (McCance, Huether, Brashers, Rote, 2010, pg. 636)
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GBS
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Tetanus
• Caused by neurotoxin tetanospasmin, elaborated by C tetani.
• Spores of the bacteria can be found in soil. Once introduced in a
wound the vegetative bacteria can produce a protease that stops
necessary proteins from facilitating neurotransmitter release.
• Tetanospasmin interferes with neurotransmission at spinal synapses
of inhibitory neurons. As a result, minor stimuli results in uncontrolled
spasms and exaggerated reflexes.
• (Papadakis & McPhee, 2013, pg. 1429)
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Clinical Manifestations • Pain, tingling, numbness at site of inoculation
• Spasticity of muscles near site of inoculation.
• Jaw, neck stiffness, dysphagia, and drooling. Spasms of the jaw muscles (trismus) or facial muscles, rigidity and spasms of the abdominal, back or neck muscles.
• Painful tonic convulsions, spasms of the glottis and respiratory muscles causing ASPHYXIA.
• Oh by the way, the patient is awake and alert through the whole illness!
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Treatment
• Prevention with tetanus and diphtheria toxoid.
• Human tetanus immune globulin within 24 hours of
presentation.
• Reduce stimuli, bed rest.
• Full ventilatory support, sedation, paralysis.
• PCN to eradicate toxin-producing organisms.
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Questions
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References
Flower, O., Wainwright, M., Caulfield, A.F., (2015). Emergency Neurological Life
Support: Actue Non-traumatic Weakness. Neurocritical Care Society.
DOI 10.1007/s12028-015-0160-7
McCance, K., Huether, S., Brashers, V., Rote, N., (2010). Pathophysiology: The
biologic basis of disease in adults and children (6th ed). Philadelphia,
PA. Elsevier
Papadakis, M., & McPhee, S., (2013). Current medical diagnosis & treatment
2013 (52ed). McGraw-Hill. New York, NY.
ENLS. 2017. OhioHealth Neuroscience Symposium.
ENS’s CEN Online Review. 2017.
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Strokes
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Head Trauma