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ri lon thc v hn m
Evaluating ED Patients Who Present with AMS & Coma
Systematic Approach
TS. CAO PHI PHONG
Cc cu hi t ra
NH NGHA V CHN
ON PHN BIT HN M
AMS & Coma: Key Concepts
Definition of Coma
Glasgow coma score of less than 10
Eyes closed unresponsiveness
@ Eye opening 1-4
@ Verbal 1-5
@ Motor 1-6
The
The RAS
RAS and
and Essential
Essential Neurotransmitters
Neurotransmitters
Epinephrine:
Locus Coeruleus
Serotonin:
Median Raphe
Acetylcholine:
Basal Nucleus
Coma Pathophysiology
Bilateral cerebral cortex dysfunction
Toxic/metabolic
Mass lesion, increased ICP
Cerebral ischemia, infarct
Acute Delirium
Delirium definition:
Mental confusion
Clouded consciousness
Disorientation, hallucinations
Delusions, anxiety (ao giac, lo u)
Incoherent speech (li noi khng mach lac)
Coma
Coma definition:
Extreme alteration in mental status
Unresponsive
Similar to being unconscious
1. Locked-in syndrome
2. Persistent vegetative state
3. Abulia (akinetic mutism )
4. Catatonia
5. Pseudocoma
TS. CAO PHI PHONG
Akinetic mutism
(a)Characteristics * State that seemingly awake, but
remains silent & motionless * Only eye dart in direction
of moving object * Despite lack of movement, few
motor signs or movement (mt nhin theo muc tiu
chuyn ng)
- Frontal release sign (sucking, grasp reflex: px bu,
cm nm)
- Move one side or one arm in stereotyped fashion
-Pyramidal sign in paralyzed limb
TS. CAO PHI PHONG
(b) Lesion
- Bilateral frontal lesion (anterior cingulate gyrus)
- Diencephalic-mesencephalic reticular formation
- Globus pallidus or hypothalamus
- Common etiology --Anoxia, head trauma,
cerebral infarction, severe acute hydrocaphalus,
Features:
-
Locked-in syndrome
(a)Features
Mute, motionless
-
(b) Lesion
- Pontine lesion
- Basilar artery thrombosis /c ventral pontine infarct,
Pontine hemorrhage, pontine tumor.
- Central pontine myelinolysis
- Midbrain lesion (bilateral ventral region):
(Bilateral ptosis & vertical, horizontal ophthalmoplegia)
CN NGUYN HN M
Coma Etiologies
Hypoperfusion/ischemia
Toxic/metabolic
Increased ICP
Chronic space-occupying lesion
Acute hemorrhage
Infection
Seizure
Psychogenic fugue state
Coma Etiologies
AEOIU-TIPS
Coma Etiologies
T trauma, temperature
I infections
P psychiatric, porphyria
S space-occupying lesion,
stroke, SAH
Coma Etiologies
A
E
I
O
U
NH GI BN HN M
nh gi bnh nhn hn m
Assess ABCs, vitals
Provide empiric therapies
Assess for signs of likely etiology
Trauma, toxic, infection, ischemia, tumor
LEVEL OF CONSCIOUSNESS
Coma Scales
Glasgow Coma Scale (GCS),
ACDU (alert, confused, drowsy, unresponsive)
AVPU (alert, response to voice, response to pain,
unresponsive)
AVPU
FOUR Score
FOUR Score
FOUR Score
Research Protocol
Aims:
1. To evaluate the use of the FOUR score
in the prehospital setting
2. To test agreement between emergency
care providers when measuring the
FOUR score
TS. CAO PHI PHONG
FOUR Score
Research Protocol-Outline
TransportingtoAGMC
EMSpatientwithGCS14
Any
etiology
Pre
H
osp
ita
PERFORMEMSFOURScore
PerformE.D.FOURScore
E.D
.
PerformI.C.U.FOURScore
IC
U
At24hours
Outcomeat30days
FOUR Score
FOUR Score
FOUR Score
FOUR Score
FOUR Score
Motor Examination
FOUR Score
FOUR Score
Brainstem Examination
FOUR Score
FOUR Score
FOUR Score
Examination of Breathing
FOUR Score
Examination of Breathing-Picture
FOUR Score
2 type of patients
Intubated or NOT intubated
YOU ARE THE VENTILATOR
FOUR Score
FOUR Score
Motor Examination-Picture
(Theo di)
NG T
PUPILLARY RESPONSES
Px nh sng
Px hi t v iu tit
Hippus
Hippus, also known as pupillary athetosis, is spasmodic,
rhythmic (< 0.04 Hz), but irregular dilating and contracting
pupillary movements between the sphincter and dilator
muscles. Pupillary hippus comes from the Greek hippos
meaning horse, perhaps due to the rhythm of the
contractions representing a galloping horse.
It is particularly noticeable when pupil function is tested
with a light, but is independent of eye movements or
changes in illumination. It is usually normal, however
pathological hippus can occur.
Hippus has been classically been noted as sign of Aconite
poisoning (ng c cy phu t)
TS. CAO PHI PHONG
OCULOMOTOR RESPONSES
RESTING AND SPONTANEOUS EYE MOVEMENTS
Ocular Motility
Cerebrum, cerebellum, and brainstem
Evaluation of ocular motility:
(1) observation of the resting position of the
eyes, including eye deviation;
(2) notation of spontaneous eye movements.
(3) testing of reflex ocular movements
TS. CAO PHI PHONG
4. Skew deviation
@ posterior fossa lesion (brainstem or
cerebellar)
@ Dysconjugate vertical eye position may
sometimes occur in the absence of a
brainstem lesion in the obtunded patient.
TS. CAO PHI PHONG
Mollaret's triangle:
gia red nucleus, inferior olives,
v dentate nucleus tiu no. Tn
thng gy palatal myoclonus
PHAN XA VN NG MT
(Reflex Ocular Movements)
RESPIRATION
Neuropathologic Correlates of Breathing
Abnormalities
Forebrain damage
Epileptic respiratory inhibition
Apraxia for deep breathing or breath
holding
Pseudobulbar laughing or crying
Posthyperventilation apnea
Cheyne-Stokes respiration
TS. CAO PHI PHONG
Hypothalamic-midbrain damage
Central reex hyperpnea
(neurogenic pulmonary edema)
Medullary dysfunction
Ataxic breathing
Slow regular breathing
Loss of autonomic breathing with
preserved voluntary control
Gasping
Apneusis: inspiratory
pauses, may be seen in
patients with bilateral
pontine lesions.
Cluster breathing and
ataxic breathing: lesions
at the pontomedullary
junction
Apnea
TS. CAO PHI PHONG
NH GI VN NG
MOTOR RESPONSES
Patients with forebrain or diencephalic
lesions often have a hemiparesis
Lesions involving the junction of the
diencephalon and the midbrain may
show decorticate posturing, including
exion of the upper extremities and
extension of the lower extremities
TS. CAO PHI PHONG
MOTOR RESPONSES
Lesion progresses into the
midbrain, there is generally a shift to
decerebrate posturing
Mt v v mt no
(Decorticate vs. Decerebrate)
Lateral
Red
Nucleus
Ventromedial
Reticular
Nuclei
Superior Colliculus
vestibular nuclei
Spinal cord
TS. CAO PHI PHONG
(--)
HE
THAP
Nhan
o
Gia c kh nng
chng trng lc
(--)
C gap chi
tren
Bo tien
nh song
C duoi
t ch
Bo li
song
Gia c trng lc
dui
TS. CAO PHI PHONG
Lesion below the level of the red nucleus but above the
level of the vestibulospinal and reticulospinal nuclei will
result in decerebrate posture
(upper extremity in pronation and extension and the
lower extremity in extension).
Empiric Therapies:
The Procedure
TS. CAO PHI PHONG
Oxygen therapy
Obtain an accucheck, administer glucose
Fluid bolus for hypotension
Naloxone if evidence of narcotic use/abuse
Judicious flumazenil use for benzo abuse
Thiamine in alcohol abuse
La chn
Empiric Therapy
Control the airway, ventilate
Empiric Therapy
Control the airway, ventilate
Do a bedside glucose determination
Provide D50 for hypoglycemia
Avoid hyperglycemia
Empiric Therapy
Control the airway, ventilate
Do a bedside glucose determination
Provide D50 for hypoglycemia
Avoid hyperglycemia
Empiric Therapy
Assess for narcotic overdose
Nalaxone 2 mg IV or sublingual
Be prepared to restrain patient
Empiric Therapy
Assess for narcotic overdose
Nalaxone 2 mg IV or sublingual
Be prepared to restrain patient
Empiric Therapy
Assess for narcotic overdose
Nalaxone 2 mg IV or sublingual
Be prepared to restrain patient
R rang
Oculocephalic reflex
Caution with suspected c-spine injury
Eyes should continue to face to ceiling
If eyes follow movement of head to side,
suspect brainstem involvement in coma
ED Documentation &
Patient Outcome
ED Coma Documentation
Pt unresponsive to all stimuli cw coma
Airway adequately controlled
Decreased gag reflex
OK Airway with nasopharyngeal airway
ED Coma Documentation
No pallor, cyanosis, or cherry red skin
No abnormal breath or EtOH
Adequate ventilation, pO2 OK 100% NRB
Hypertension noted, tachycardia
Labetalol 20 mg IVP
Repeat BP OK
ED Coma Documentation
Corneal reflex intact, no upgoing toes bilat
Pupils midrange, equal, reactive
Fixed gaze to R, no Dolls eyes noted
Protective reflex to arm dropping absent
No propriety reflex noted
Facial twitching noted on R, likely SE
Cold calorics not indicated
TS. CAO PHI PHONG
ED Coma Documentation
Coma
Likely etiology subtle status epilepticus
No toxidrome or intoxication
Non-focal exam, mass lesion not likely
No evidence psychogenic seizure
CT negative, tox screen negative
Lorazepam, fosphenytoin
EEG negative in ED
TS. CAO PHI PHONG
Patient Outcome
Hx SE, compliant with meds?
Hx carotid occlusion
Due to have carotid endarterectomy
Pt remained unresponsive after EEG
Admitted for ongoing observation
Expedited surgery anticipated
TS. CAO PHI PHONG
Questions??