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Neurologic Emergencies

StATUS EPILEPTICUS
& OTHERS SEIZURES DISORDER
dr. IGN Budiarsa, SpS
NEUROLOGY DEPARTMENT/MEDICAL FACULTY
OF UDAYANA UNIVERSITY/Sanglah HOSPITAL
Denpasar

seizures
Abnormal electrical discharge
of neurons causing a clinical
episode of neurologic
dysfunction.

CLASSIFICATION
Generalized
Tonicclonic (grand
mal)
Absence
(petit mal)
Myoclonic
Clonic

Tonic
Atonic
Partial (focal)
Simple partial
Complex partial
Aura

Todds paralysis: Focal neurological


deficit persisting from seizure, which
usually resolves within 48 hours.

MANAGEMENT
Position
Patients having a seizure should be rolled to a
semiprone position to allow gravity to pull the tongue
and secretions out of the airway. The head should be
aligned with the body, and nothing should be put in the
mouth.
ABCs
Airway: Maintain adequate airway with nasal trumpet.
Breathing: Administer oxygen.
If properly positioned, cyanosis and apnea are rare.
Circulation: Obtain IV access.

MANAGEMENT
History
Important history can be obtained from
by standers or witnesses.
Include syncope as part of your
differential diagnosis.
Seizures can cause loss of bladder
control.
Differentiate between partial and
generalized seizure (ask patient if they
can recall event).

MANAGEMENT
History
First seizure or known seizure history.
Baseline seizure history (frequency and
last seizure episode).
Recent history of trauma.
Consider factors that may lower seizure
threshold (alcohol/drug withdrawal,
illness, sleep deprivation).

Factors that lower seizure


threshold: I AM H4IP

Infection
Alcohol withdrawal, drugs
Medication (changes in dosing or compliance)
Head injury, Hypoxia,
Hypoglycemia,
Hypertension,
Hyponatremia (and other electrolyte abnormalities
[Ca+ Mg])
Intracranial lesions
Pregnancy (eclampsia)

SIGNS AND SYMPTOMS


Physical Exam
Check for injuries caused as
a result of seizure activity.
Look for signs of infection,
especially CNS infections.
Assess and reassess mental status for
signs of deterioration.

DIAGNOSIS
Routine labs.
Magnesium, calcium, toxicology screen,
alcohol level, liver function tests.
Consider LP.
Consider CT scan of head.

TREATMENT
Prevention of injury and adequate oxygenation in
the actively seizing patient.
Benzodiazepines are the mainstay of treatment in
the seizing patient.
Correct subtherapeutic levels of anticonvulsants.
Treat underlying causes (meningitis, hypoglycemia,
etc.).
Most often, treatment is mainly supportive.
IV fosphenytoin, valproic acid, or phenobarbital if
benzodiazepines fail.

PRIMARY SEIZURE DISORDER


Some due to genetic defect in
channel proteins.
0.5 to 1% of population has disease.
Epilepsy: Diagnosed after two or
more unprovoked seizures.

SECONDARY SEIZURE DISORDER


DEFINITION
Seizures that occur as a result of
another disease condition.
CAUSES
Metabolic:

Hyper/hypoglycemia
Hyper/hyponatremia
Uremia
Hypocalcemia

Infection:
Meningitis
Encephalitis
Intracerebral abscess

SECONDARY SEIZURE DISORDER


CAUSES
Trauma:
Subdural hematoma
Epidural hematoma
Intracerebral hemorrhage
SAH

Toxic:
Theophylline
Amphetamines
Cocaine
Tricyclic antidepressants
Alcohol withdrawal
CO
Cyanide

SECONDARY SEIZURE DISORDER


CAUSES
Eclampsia
Neurologic:
Cortical infarction
Intracranial hemorrhage
Hypoxia
Hypertensive encephalopathy
Congenital cerebral malformation or
cortical dysplasia

STATUS EPILEPTICUS
DEFINITION
Seizures occurring continuously for at least
30 minutes, or two or more seizures
occurring without full recovery of
consciousness between attacks.

Patofisiologi
Ketidakseimbangan
antara inhibisi (GABA)

gamma aminobutyric
acid dan eksitasi
(Glutamat)
Defisiensi neurotransmiter
inhibitor dan peningkatan
neurotransmiter
eksitatator menyebabkan
terjadi aktivitas neuron
tidak normal dikorteks

(Browne TR,Holmes GL, 2000; Chen JW, 2006)

Aktifitas Glutamat pada


reseptornya AMPA (alpha
amino 3 hidroksi 5
methylosoxale-4-propionic
acid) dan NMDA (n-methil daspartat) memicu
pembukaan kanal Na
Diikuti dengan pembukaan
kanal Ca
banyak masuk ke intrasel
Terjadi pengurangan
perbedaan polaritas pd
membran sel
Depolarisasi

(Browne TR,Holmes GL, 2000; Seeck, 1998))

Depolarisasi yg berkepanjangan
akibat peningkatan Glutamat
terjadinya potensial aksi yg terusmenerus dan memicu aktivitas sel2
saraf

(Browne TR,Holmes GL, 2000)

STATUS EPILEPTICUS
TREATMENT
Treat with IV benzodiazepines,
fosphenytoin, valproic acid, or
phenobarbital.
General anesthetics are last-line agents.

STATUS EPILEPTICUS MANAGEMENT


(PERDOSSI GUIDELINES 2012)
STADIUM & MANAGEMENT
STADIUM I (0-10 Minutes)
Cardio respiration management
Airway maneuvers, oxygenation, resuscitation (if needed)
STADIUM II (1-60 Minutes)
Neurological status examination
Blood pressure, pulse rate, and temperature measurement
Metabolic status, blood gas analysis, hematological status monitoring,
ECG
Intra venous fluid in large blood vessel with NaCl 0,9%. Two i.v line
needed if using 2 type of AED
Taking 50-100 cc blood sample for laboratory investigation (BGA,
Glucose, liver and renal function, calcium, magnesium, complete blood
count, blooding time, AED serum level), others investigation depending
to the clinical condition
Emergency AED: Diazepam 0,2 mg/kg in 5 mg/minutes i.v, could be
repeated if seizures still happening over 5 minutes
50 cc glucose 50% in hypoglycemia condition
Thiamin 250 mg i.v in alcoholism
Acidosis management with bicarbonate

STATUS EPILEPTICUS MANAGEMENT


(PERDOSSI GUIDELINES 2012)
STADIUM & MANAGEMENT
STADIUM III (0-60/90 Minutes)
Etiology determination
If seizures still happen after lorazepam/diazepam administration give
Phenytoin 15-20 mg/kgBW in < 50 mg/minutes (need blood pressure
and ECG monitoring). If seizures still happen Phenytoin could be added
5-10 mg/kgBW. If seizures continues give Phenobarbital* 20 mg/kgBB
in 50-75 mg/minutes (respiration monitoring while administration).
Could be repeated 5-10 minutes/kgBW.
Vasopressor therapy (Dopamin) if needed
Complication management
*) intubation facility must prepared
STADIUM IV (1-60 Minutes)
If seizures continues after 30-60 minutes, transfer patient to ICU, give
propofol (2 mg.kgBW iv, repeated if needed) or midazolam (0,1
mg/kgBW in 4 mg/minutes) or Tiopentone (100-250 mg iv in 20
minutes, continue with 50 mg iv every 2-3 minutes), followed until 1224 hours after clinical seizure or last EEG seizure, and than tappering
off.
Monitoring of seizures, EEG, intracranial pressure, start with AED

ECLAMPSIA
Usually occurs in patients > 20 weeks
gestation.
Present with hypertension, edema,
proteinuria, headache, vision changes,
confusion, and seizure.
Magnesium sulfate can be used to treat
eclampsia.

DELIRIUM TREMENS
Seizures can occur in alcohol withdrawal.
Associated with autonomic hyperactivity.
Seizures can occur within 6 hours after
last drink.
Treated with benzodiazepines and
supportive care.

Neurologic Emergencies

Coma & Others


Mental status changes
dr. IGN Budiarsa, SpS
NEUROLOGY DEPARTMENT/MEDICAL FACULTY
OF UDAYANA UNIVERSITY/Sanglah HOSPITAL
Denpasar

MENTAL STATUS
CHANGES
Change in mental status is a
term used to describe a
spectrum of altered
mentation including
dementia, delirium,
psychosis, and coma.

COMA
DEFINITION
Diffuse brain failure leading to
impaired consciousness.

Coma
Consciousness requires arousal
(coming from the brainstem
reticular formation) and content
(the cerebral hemispheres)
Alterations in consciousness stem from:
Disorders affecting the reticular
formation
Disorders affecting both cerebral
hemispheres
Disorders affecting the connections
between the brainstem and the

Anatomic correlation of
consciousness
Widespread
damage in both
hemispheres
Global
suppression of
cerebral function
Conscious levelless
severe

Conscious level-severe

Brainstem
lesions that
cause

Glasgow Coma Scale


Three components. Score derived
by adding the score for each
component.
Eye opening (4 points)
Verbal response (5points)
Best motor response (6 points)

Glasgow Coma Scale


Eye opening

4
3
2
1

spontaneous
to speech
to pain
none

Best Motor Response

Verbal Response

5 - oriented
4 - confused conversation
3 - inappropriate words
2 - incomprehensible
sounds
1 - none

6 - obeys
5 - localizes
4 - withdraws
3 - abnormal
flexion
2 - abnormal
extension
1 - none

Causes of Coma AEIOU


TIPS
Alcohol
Encephalopathy, endocrine (thyroid disease,
etc.), electrolyte abnormality
Insulin-dependent diabetes
Opiates, oxygen deprivation
Uremia
Trauma, temperature
Infection
Psychosis, porphyria
Space-occupying lesion, stroke, SAH, shock

MANAGEMENT
ABCs:
Airwayintubate if necessary to protect airway.
Breathingoxygen, oral airway.
Circulationintravenous (IV) access, blood
pressure.
C-spinecervical collar unless absolutely sure no
history of trauma.

Vitalstemperature, oxygen saturation (fifth


vital sign) frequent re-assessment.
Electrocardiogram (ECG)/cardiac monitor
arrhythmias, myocardial infarction (MI).

History

From patient, family member,


bystander, or old chart.
Past medical history.
Past psychiatric history.
Medications.
Social history (drug or alcohol use).

Physical exam:
General exam:
Check for signs of trauma.
Glasgow Coma Scale.
Respiratory pattern:

CheyneStokes: Periodic fluctuations of respiratory rate


and depth suggest CNS pathology.

Ocular exam:
Pupillary function: If pupils are reactive to light
bilaterally, midbrain is probably intact:
Pinpoint pupils suggest opioid toxicity or pontine
dysfunction.
Fixed and dilated pupils suggest increased intracranial
pressure (ICP) with possible herniation.

Physical exam:
Ocular motions:
Dolls eyes reflex: Turn patients head
quickly to one side and observe eye
movement. In a normal response, the
eyes move in the opposite direction.
Absence of motion suggests
dysfunction in hemisphere or brain
stem function. (Note that this reflex is
also absent in a conscious patient.)
Neurological exam: Refer to section on
neurological examination.

Diagnosis
Arterial blood gas: Acidbase disorders can help
point to etiology (remember MUDPILES).
Routine labs: Look for infection or electrolyte
abnormalities.
Toxicology screen: Look for drugs and alcohol.
X-rays: C-spine in suspected cases of trauma.
Head CT: Look for intracranial pathology.
Lumbar puncture (LP): Look for SAH or infection.
Remember, CT before LP for mass lesion/cerebral
edema/hydrocephalus.

Treatment
Coma cocktail.
Supportive care.
Monitoring (cardiac,
oxygen saturation).
Identify specific cause and
apply appropriate
treatment.
Appropriate specialty
consult as deemed
necessary.

Differentiating Delirium, Dementia, and Psychosis

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