KEGAWATDARURATAN

NEUROLOGI
Dr. dr. NOVA DIAN LESTARI, Sp.S(K)
 Outline
CEREBROVASCULAR DISEASES (CVD)
– Stroke Iskemik
– Stroke Hemoragik
– Hipertensi Emergensi
TRAUMA
– Traumatic Brain Injury
– Trauma Medula Spinalis
STATUS EPILEPTIKUS
INFEKSI SSO
– Meningoencephalitis
– Tetanus
GANGGUAN OTONOM
– SGB/GBS
 Stroke
• Blood supply to areas of the brain is
interrupted, causing ischemia
• Goal of treatment: early recognition and
rapid, appropriate intervention
 Pathophysiology of Stroke
• Neurologic conditions can have a vascular
origin.
– Typically result of emboli or aneurysms
 Pathophysiology of Stroke
• Aneurysm development process:
– Small tears occur within the arterial wall.
– Blood enters between the layers of the artery.
– Pressure builds up, and the tear increases.
– If damage is severe, the artery can leak or fail.
 Pathophysiology of Stroke
• Ischemic stroke
– A blood vessel becomes blocked, causing tissue
beyond it to become ischemic.
– The severity is dictated by:
• Artery involved
• Portion of the brain being denied oxygen
 Pathophysiology of Stroke
• Hemorrhagic stroke
– Tend to get worse over time
• Bleeding causes increased ICP and brainstem
herniation.
– Primary symptom: “worst headache of my life”
Pathophysiology of Stroke
 Assessment of Stroke
• Language effects • Movement effects
– Slurred speech – Hemiparesis
– Aphasia – Hemiplegia
– Agnosia – Arm drifting
– Apraxia – Facial droop
– Tongue deviation
– Swallowing difficulties
– Ptosis
– Ataxia
 Assessment of Stroke
• Sensory effects • Cognitive effects
– Headache (hemorrhagic) – Decreased LOC
– Sudden blindness – Difficulty thinking
– Sudden unilateral – Seizures
paresthesia – Coma
• Cardiac effects
– Hypertension
 Stroke
Iskemik
Stroke Hemoragik
 Management of Stroke
• Administer fluids as needed.
• Elevate the patient’s head 30°.
• Ensure airway is clear.
• Watch for seizures.
• Monitor blood pressure closely.
 Management of Stroke
• High oxygen level constricts arteries.
• Lower level of carbon dioxide lowers ICP.
– Ventilation decreases CO2 and increases O2.
• Provide ventilatory support at 16 to 20 breaths/min.
• Maintain PET CO2 in high 20s to low 30s mm Hg.
Management
of Stroke
 Management of Stroke
• Transport decisions
– Transport to stroke centers.
– If you suspect hemorrhagic stroke, consider a
facility that can perform neurosurgery.
• Call ahead to ensure rapid evaluation.
Hypertensive Emergencies
• CNS - Hypertensive encephalopathy
• CVS
– Acute myocardial ischemia
– Acute cardiogenic pulmonary edema
– Acute aortic dissection
– Post-op vascular surgery
• Renal - Acute renal failure
• Eclampsia
• Catechol excess- Pheochrom, Drugs
 Hypertensive Emergencies
• High BP WITHOUT acute end-
organ dysfunction IS NOT a
hypertensive emergency
• “Hypertensive Pseudoemergency”
 Cerebral Blood Flow
• CBF = CPP / CVR
• CPP = MAP - ICP
• MAP = DBP + 1/3 PP
• Cerebral autoregulation
– normal between 50 - 150
– 70/40 to 190/130
• Vascular stenosis
 Cerebral Autoregulation

CBF
50
ml/100g/min

50 150
MAP
 Cerebral Autoregulation
• Shift to right
– Chronic hypertensives
– ICH, SAH, Ischemic infarct
– Trauma
– Cerebral edema
– Age, atherosclerosis
• Some hypertensives suffer decrease CBF
at MAP higher than 120
 Cerebral Autoregulation
• CPP below lower limit
– hypoperfusion with ischemia
• CPP above upper limit
– “breakthrough” vasodilation
– Segmental pseudospasm
(“sausage-string”)
– fluid extravasation
Pathophysiology of Hypertensive
Emergencies
• Rate of change of BP determines
likelihood
• Chronic HTN lowers probability
– adaptive vascular changes protect end-
organs from acute changes in BP
• Previous normotensives (eclampsia,
acute GN) develop signs and
symptoms at lower BP’s
 Pathophysiology of Hypertensive
Emergencies
• Endothelial Role in BP Homeostasis
– Secretion of vasodilators (NO, Prostacyclin)
• Sudden increased vasoreactivity
– norepinephrine, angiotensin II
– activation of renin-angiotensin-
aldosterone
 Therapeutic considerations in
hypertensive emergencies
• Need for rapid reduction of BP
• Potential complications of therapy
– Prevalence of cerebrovascular disease
and coronary artery disease (Stenotic
lesions)
– Altered cerebral autoregulation
– Impaired baroreflexes
– Blood viscosity
– Ability to increase oxygen extraction
 How far can BP be safely
lowered?
• Lower limit usually 25% below MAP
• 50% of chronic hypertensives reached
lower autoregulation limit with 11 to
20% reduction in MAP
• 50% had lower limit above usual mean
– Kanaeko et al; J Cereb Blood Flow Metab 3:S51,1983
• Most ischemic complications develop
with reductions greater than 20 - 30 %
(over 24 to 48 hours)
• Blindness, paralysis, coma, death, MI
 Initial Lowering of BP :
Therapeutic Guidelines
• Do not lower BP more than 20% over
the first 1 to 2 hours unless necessary
to protect other organs
• Decreasing to DBP of 110 or patients
“normal” levels may not be safe
• Further reductions should be very
gradual ( days)
• Follow neuro status closely
 Traumatic Brain Injury
• Classified into:
– Primary brain injury
• Injury to the brain and its associated structures
– Secondary brain injury
• After-effects of primary injury
 Traumatic Brain Injury
• The most common
cause is a motor
vehicle crash.
• Coupe-contrecoup
– Front-and-rear type
of injury
 Intracranial Pressure
• An increase in ICP can be caused by:
– Accumulation of blood within the skull
– Swelling of the brain
• Increase in ICP decreases cerebral perfusion
pressure (CPP) and blood flow.
– CPP = MAP - ICP
 Intracranial Pressure
• Early warning signs of • Ominous signs:
ICP: – Hypertension
– Vomiting – Bradycardia
– Headache – Cushing triad
– Altered level of – Nonreactive pupil
consciousness – Coma
– Seizures – Posturing
• Decorticate
• Decerebrate
 Diffuse Brain Injuries
• Cerebral concussion
– Brain is jarred around in the skull.
– Signs include:
• Confusion, disorientation
• Loss of consciousness
• Retrograde amnesia
• Autograde (posttraumatic) amnesia
 Diffuse Brain Injuries
• Diffuse axonal injury (DAI)
– Associated with or similar to a concussion
– Involves stretching, shearing, tearing of nerve
fibers and axonal damage
– Classified as mild, moderate, or severe
 Focal Brain Injuries
• Cerebral contusion
– Brain tissue bruised and damaged in local area
– Greater neurologic deficits
– Swelling of the brain leads to increased ICP.
 Focal Brain Injuries
• Intracranial
hemorrhage
– Epidural hematoma
• Accumulation of
blood between skull
and dura mater
• Result of blow to
the head
 Focal Brain Injuries
• Intracranial
hemorrhage
(cont’d)
– Subdural hematoma
• Accumulation of
blood beneath dura
mater outside the
brain
• Associated with
venous bleeding
• Acute or chronic
 Focal Brain Injuries
• Intracranial
hemorrhage
(cont’d)
– Intracerebral
hematoma
• Bleeding in brain
tissue
• Patient’s condition
deteriorates quickly.
 Focal Brain Injuries
• Intracranial hemorrhage (cont’d)
– Subarachnoid hemorrhage
• Bleeding into subarachnoid space
• Patient presents with sudden, severe headache.
 Focal Brain Injuries
• Intracranial hemorrhage (cont’d)
– Subgaleal hemorrhage
• Bleeding between periosteum and galea aponeurosis
– Supragaleal hemorrhage
• Firm, nodular mass
EDH
 Assessment and Management
• Should be guided by
factors such as:
– Severity of injury
– Patient’s level of
consciousness
 Assessment and Management
• Thermal management
– Do not allow patient to develop hyperpyrexia.
• Treatment of associated injuries
– Apply loose, sterile dressings.
– Objects impaled should be stabilized.
 Assessment and Management
• Pharmacologic therapy
– May be ordered if transport will be prolonged
– Benzodiazepines should be used for seizures.
– No neuroprotective agents are currently
administered in a prehospital setting.
Pathophysiology, Assessment, and Management
of Spine Injuries
• Spinal cord injury (SCI) has limited treatment
options.
– Reducing incidence is best option for decreasing
associated morbidity and mortality.
 Flexion Injuries
• Result from forward
movement of head
• Typically result of
rapid deceleration
or direct blow to
occiput
 Rotation with Flexion
• The only area of the
spine that allows for
rotation is C1–C2.
• Injuries are
considered
unstable.
 Vertical Compression
• Transmitted through
vertical bodies
• Result from direct blow
to crown or rapid
deceleration from a fall
 Hyperextension
• Results in fractures
and ligamentous
injury of variable
stability
 Primary Spinal Cord Injury
• Occurs at moment of impact
• Spinal cord concussion
– Temporary dysfunction lasts 24 to 48 hours.
– May be due to a short-duration shock or pressure
wave within the cord
 Primary Spinal Cord Injury
• Spinal cord contusions
– Caused by fracture, dislocation, or direct trauma
• Cord laceration
– Caused when a projectile or bone enters the
spinal canal
 Secondary Spinal Cord Injury
• Occurs when multiple factors permit a
progression of the primary SCI
• Classified as either complete or incomplete
 Secondary Spinal Cord Injury
• Anterior cord syndrome
– Displacement of bony fragments into anterior
portion of the spinal cord
– Findings include paralysis below level of insult
• Central cord syndrome
– Hyperextension injuries to the cervical area
– Loss of function in upper extremities
 Secondary Spinal Cord Injury
• Posterior cord syndrome
– Associated with extension injuries
– Presents as decreased sensation to:
• Light
• Touch
• Proprioception
• Vibration
 Secondary Spinal Cord Injury
• Cauda equina syndrome
– Compression of bundle of nerve roots
– Can produce the following:
• Low back pain
• Myalgia, paresthesia, or myasthenia
• Loss of sensation
• Acute bladder/bowel dysfunction
 Secondary Spinal Cord Injury
• Brown-Séquard syndrome
– Functional hemisection of the cord; complete
damage to spinal tracts on involved side
• Spinal shock
– Temporary local neurologic condition that occurs
immediately after spinal trauma.
 Secondary Spinal Cord Injury
• Neurologic shock
– Results from temporary loss of autonomic
function at the level of injury
– Hemodynamic and systemic effects are seen.
 Assessment and Management
• Current principles of spine trauma
management include:
– Recognition of potential or actual injury
– Appropriate immobilization
– Reduction or prevention of secondary injury
 Assessment and Management
• Patient may not require immobilization if:
– No neurologic deficit
– Not under influence of alcohol, drugs, or
medications
– No distracting injuries
– No motor or sensory deficit
– No pain or tenderness
Spinal Splinting Procedures for Supine
Patients
Spinal Splinting Procedures for Supine
Patients
• Do not force the head into a neutral, in-line
position if the patient has:
– Muscle spasms in the neck
– Increased pain with movement
– Numbness, tingling, or weakness
– Compromised airway or ventilation
Spinal Splinting Procedures for Seated
Patients
• A rigid cervical collar should be measured and
placed appropriately.
• A vest-type board should be used to transfer
the patient onto a long backboard.
Spinal Splinting Procedures for Seated
Patients
 Spinal Splinting Procedures for Rapid
Extrication
• Use in the following situations:
– Vehicle or scene is unsafe
– Patient cannot be assessed before being removed
from the car.
– Patient needs immediate intervention.
– Patient’s condition requires immediate transport.
– Patient blocks access to another injured patient.
Spinal Splinting Procedures for Rapid
Extrication
Spinal Splinting Procedures for
Standing Patient
 Packaging and Removal of Injured
Patients from the Water
• Assume spinal injury for the following:
– Diving injury
– Boating injury
– Watercraft injury
– Falls from heights
Packaging and Removal of Injured
Patients from the Water
 Patients Wearing Helmets
• Helmet removal is recommended in the
following situations:
– Helmet and chin strap fail to hold head securely.
– Helmet and chin strap prevent airway control.
– Helmet with a face mask cannot be removed.
– Helmet prevents proper immobilization.
Patients Wearing Helmets
Pharmacotherapy of Spinal Cord Injury
• Short-acting, reversible sedatives are
commonly recommended for acute agitation.
• Pain medication may be necessary.
• Corticosteroids are sometimes used in the
acute phase of SCI.
Complications of Spinal Cord Injury
• Potential for aspiration or respiratory arrest
• Predisposal to atelectasis and pneumonia
• Deep vein thrombosis and pulmonary
embolism
Complications of Spinal Cord Injury
• Autonomic dysreflexia
– Potentially life threatening
– Most commonly occurs with injuries above
T4–T6
– Patients present with a massive, uncompensated
cardiovascular response.
Complications of Spinal Cord Injury
• Autonomic dysreflexia (cont’d)
– Common precipitators include:
• Skin lesions
• Constrictive clothing
• Sharp objects compressing the skin
– Management is usually not a prehospital
intervention.
 Status Epilepticus
• Pathophysiology
– Seizure that lasts longer than 4 to 5 minutes or
consecutive seizures
• May result in neurons being damaged or killed
– Goal: stop seizure and ensure adequate ABCs.
 Status Epilepticus
• Assessment
– Same as for a seizure
• Management
– Administer a benzodiazepine.
– Be prepared to control airway and ventilation.
– Paralytics may be needed.
 Generalized Convulsive Status Epilepticus

• Rapid diagnosis
– History: epilepsy, other neurologic disease,
diabetes, drug ingestion/withdrawal, infectious
symptoms, pre-seizure neurologic symptoms
– Exam:
• subtle signs of ongoing seizure (periorbital/perioral
clonus, forced horizontal conjugate eye deviation,
hippus)
 Generalized Convulsive Status Epilepticus

• Rapid diagnosis
– Imaging: CT for associated mass lesion
– Labs: glucose, electrolytes, urine and serum
toxicology screens
– CSF
• Evidence of infection OR
• No other clear cause from history, exam, CT, and labs
 Generalized Convulsive Status Epilepticus

• Seizures beget seizures

– Early treatment = higher chance of success
– Balance this with side effects of treatment (need
for intubation, hypotension)
• Excitotoxic neuronal death
 Lactic and Cardiac Rhabdomyolysis
respiratory arrhythmias
acidosis

pH 
pCO2 
Lactate  Myoglobinuria
Status epilepticus

Aspiration Pulmonary Shoulder Rib

pneumonia edema dislocation fracture CP1142808-43
Figure courtesy of Dr. Eelco F.M. Wijdicks
Emergency Treatment of Generalized Convulsive
Status Epilepticus
• Abort the seizure
– Lorazepam 4-6mg IV push
– Repeat 5min later if seizure continues or returns

• Prevent future seizures

– Phenytoin load: 20mg/kg IV infusion
– DO NOT just give 1g  only enough for a small, 50kg
person
– Alternatives:
• IV valproic acid 20-30mg/kg
• IV levetiracetam 25-30mg/kg
 CNS Infections/Inflammation
• Pathophysiology
– Encephalitis: inflammation of the brain
– Meningitis: inflammation of the meninges
– Damage is caused by:
• Body’s reaction to the infection, or
• Activities of the attacking organisms
 CNS Infections/Inflammation
• Pathophysiology (cont’d)
– If temperature becomes too high, a person may:
• Hallucinate
• Become delusional
• Lose consciousness
• Have a febrile seizure
 CNS Infections/Inflammation
• Pathophysiology (cont’d)
– Proteins that damage cells
• Endotoxins: released by gram-negative bacteria
• Exotoxins: secreted by some bacteria or fungi
– Virus attacks the axons.
 CNS Infections/Inflammation
• Assessment

© Jones & Bartlett Learning

– Both illnesses begin
with flulike
symptoms.
– Meningitis may
elicit:

© Jones & Bartlett Learning

• Kernig’s sign
• Brudzinski’s sign
 CNS Infections/Inflammation
• Management
– If meningitis is suspected:
• Place a mask over the patient’s mouth.
• Wear a mask if the patient is coughing.
– Be prepared for seizures.
 CNS Infections/Inflammation
• Management (cont’d)
– Paramedic may need antibiotic treatment.
– Hospital treatment includes:
• Decreasing swelling in the brain and spinal cord
• Fighting the infection
• Supporting the patient’s vital signs
 Guillain-Barré Syndrome
• Pathophysiology
– Disease in which the immune system attacks
portions of the nervous system
– May report previous respiratory or GI infection
– Some patients recover completely; others require
assistance for the rest of their lives.
 Guillain-Barré Syndrome
• Assessment
– Begins as weakness in the legs
• Moves up the legs and affects the thorax and arms.
• Can lead to paralysis
– Patients are prone to severe swings in pulse rate
and blood pressure.
 Guillain-Barré Syndrome
• Management
– Assess ability to protect the airway.
– Monitor closely with ECG.
– Repeat vital signs.
– Obtain continuous end tidal CO2 readings.
– Be prepared to administer IV fluids.
– Provide comfort.
 Guillain-Barre Syndrome
• CSF: cytoalbuminological dissocation (elevated protein
with few or no mononuclear cells)
• May be normal in the first week
• If WBC count >10 consider Lyme, HIV, sarcoidosis
• Electromyography/nerve conduction study
• Reduced nerve conduction velocities
• Conduction block
• Prolonged F-waves
• Antiganglioside antibodies
• GM1 Abs (correlate with C. jejuni infection)
• GQ1b associated with C. Miller Fisher variant (ataxia,
areflexia & ophthalmoparesis)

94
 Guillain-Barre Syndrome

• Typically follows an • Areflexia

infectious process (2/3) • Autonomic dysfunction
– C. jejuni, CMV, EBV, M. – Labile BP, arrhythmia
pneumoniae – Bowel and bladder
• Presents with ascending function typically spared
numbness/tingling, can • Symptoms should not
be painful proceed >8 weeks
• Weakness typically – 98% achieve “plateau
follows sensory phase” by 4 weeks
disturbances – Duration of “plateau” 12
days

95
 Treatment
• Telemetry, respiratory parameters, ICU monitoring
for dysautonomia and respiratory compromise
• IVIG (0.4g/kg/day for 5 days) versus plasma exchange
– Ease of administration, fewer complications, preferred in
hemodynamically unstable patients
– Should be started within 2 weeks
• Corticosteroids have not been shown to be beneficial
• Intubation criteria:
– VC <15-20 mL/kg (<30% baseline)
– PO2<70 mmHg
– Oropharyngeal weakness, weak cough, suspected
aspiration

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GBS vs Acute Myelitis Transvere
TERIMA KASIH