Evaluation of Altered
Mental Status
Kalpesh Patel, MD
Dept. of Pediatric Emergency
Medicine
October 25, 2006
Objectives
 To understand the different terms used for level of
consciousness.
 To understand to pathophysiology behind altered
level of consciousness (ALOC).
 To review the differential diagnosis for ALOC.
 To learn important physical exam findings to clue
you into the etiology of ALOC.
 To review the basic management of ALOC.
2
Definitions
 Consciousness defined as being awake and aware
of both one’s self and one’s surroundings.
• Age specific responses
 Altered Consciousness covers a spectrum of
states:
• Consciousness
• Coma
• Lethargy
• Confusion/Disorientation
• Stupor or Obtunded
3
Definitions
 Consciousness
 Confusion/Disorientation – occurs in the order of
time, place, person, then unconsciousness
 Stupor or Obtunded – not totally asleep, but
diminished response to external stimuli
 Lethargy – Depressed consciousness like a deep
sleep state where pt roused, but immediately
returns to deep sleep
 Coma – complete unawareness and
unresponsiveness
 States change over time, so pt specific responses
are preferable descriptors
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Epidemiology
 Bimodal distribution
 Infection accounts for 1/3 of nontraumatic cases
 Congenital malformations present in the first few
postnatal months
 DKA more common in adolescence
 Inborn errors present in infancy
 Toxic ingestion common in childhood and
adolescence
 Rate of trauma increases throughout childhood
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Pathogenesis
 Cerebral hemispheres –
cognition, affect, perception
of themselves and
environment
 Wakefulness – Ascending
Reticular Activating System
(ARAS)
• Midbrain/pons
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Pathogenesis
 Near cranial nerves II, III,
VI, and VIII and MLF
• Controls pupillary light
reflexes and eye
movements
 Impingement of cranial
nerves suggests
impingement of ARAS
 Pupillary responses
proved the most direct
window to the brain
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Pathophysiolgy
 Compression of the ARAS usually results from
structural causes
 Diffuse cerebral dysfunction usually has a medical
basis
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Etiologies
 Altered Level of Consciousness (ALOC):
• One of the most difficult diagnostic and
management problems in pediatric emergency
medicine
• Requires quick action to avoid irreversible
damage
• Wide array of possible diagnoses
 ALOC is a symptom of another problem, not a
diagnosis itself
 Helpful mnemonic is AEIOU TIPS
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Etiologies
 A – Alcohol, Abuse (physical or substance)
 E – Encephalopathy, Electrolytes
 I – Insulin, Intussusception, Inborn errors
 O – Overdose, Oxygen deficiency
 U - Uremia
 T – Trauma, Temperature abnormality, Tumor
 I - Infection
 P – Poisoning, Psychiatric, Psychogenic
 S – Shock, Stroke, Seizures, Shunt
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Herniation Syndromes
 Increased ICP
• Found in many etiologies causing space occupying lesions
• Requires immediate identification and action
 Focal neurologic signs suggest a structural lesion, lack of
focality suggests a medical cause
• Exceptions:
 Acute hydrocephalus
 Bilateral subdural hematomas
 Acute bilateral cerebrovascular disease
 Encephalopathies with focal signs
 Postictal states such as Todd paralysis
 Beware of Cushing’s triad – hypertension, bradycardia,
irregular respirations
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Herniation Syndromes
 Central herniation
• Pressure in both
hemispheres
• Pushes midbrain and
upper brainstem through
tentorium
 Foramen Magnum
(Tonsillar) herniation
• Posterior fossa pressure
• Pushes cerebellar tonsils
through foramen
magnum
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Herniation Syndromes
 Cingulate gyrus herniation
• Unilateral cerebral
hemisphere pressure
• Pushes gyrus beneath
falx cerebri
 Uncal herniation
• Unilateral volume
increase
• Pushes lower midline
cerebrum and
hippocampal gyrus
through tentorium
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ALOC Clinical Features
 4 pathophysiologic variables are helpful
• Respiratory pattern
• Pupillary light reflexes
• Spontaneous eye movements
• Motor responses
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Respiratory Pattern
 Ventilation is governed by lower pons and medulla
• Modulated by forebrain cortical centers
 Patterns from rostrocaudal involvement
• Post-ventilation apnea
 lasts 10-30 sec followed by voluntary deep
breathing
 Forebrain involvement
• Cheyne Stokes respirations
 Hyperpnea alternating with apnea
 Depth of breathing crescendo-decrescendo
 Diencephalon of deep cerebral hemispheres
 Caused by failing respiratory center of brain
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Respiratory Pattern
 Central neurogenic hyperventilation
• Regular and rapid respirations
• Normal PaO2 and low PaCO2
• Midbrain
• Brain’s attempt to reduce ICP
 Apneustic breathing
• Deep, gasping inspiration with a pause at full
inspiration followed by a brief, insufficient release
• Signifies damage to Pons/medulla
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Pupillary Reflex
 Pupillary pathways near ARAS
 Pupillary pathways resistant to metabolic insult
 Single most important physical finding to distinguish
structural vs metabolic disease
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Pupillary Reflex
 Unequal, sluggish or
unreactive pupils (1)
 Eye is affected is on the side of
the lesion (2)
 Bilateral enlarged and
unreactive pupils indicate
massive CNS dysfunction (3)
 Drugs also affect pupils
• Opiates – pinpoint pupils
• Anticholinergics – large
pupils
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Eye Movements
 In light stage of coma, roving side-to-side
movements occur
 Persistent deviation to one side may indicate focal
seizure activity
 Structural brainstem lesions abolish conjugate eye
movements
 Oculocephalic reflex (“doll’s eyes”) – hold eyelids
open and rotate head from side to side
• Normal or positive – conjugate deviation of eyes
away from direction of head movement
• Contraindicated in c-spine injury
•
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http://prohealthsys.com/physical/movies/cranialnerve_n_13.mov
Eye Movements
 Oculovestibular reflex – elevate head of bed 30
degrees and inject 10-50ml of ice water into ear
canal
• Normal response is nystagmus with slow phase
towards irrigated ear and fast beats away
• Unconscious pt with intact brainstem eyes move
towards stimulus and remain tonically deviated
for a minute and slowly return to midline
• Contraindicated if tympanic membrane not intact
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Eye Movements
 Cerebral lesions – eyes deviated towards side of
lesion
 Brainstem lesions – eyes deviated away from side
of lesion
 Setting sun sign – downward deviation of eyes
• Upper midbrain lesions and hydrocephalus
 Third nerve paralysis – eyes point down and out
•
http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm
 Brief fundoscopic exam should also be performed
looking for papilledema or retinal hemorrhages.
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Motor Responses
 Assess muscle strength, tone and deep tendon
reflexes for normality and symmetry
 Assess if pt can localize motor responses to
determine level of brain lesion
• Decerebrate posturing – flexion of upper
extremities with extension of lower extremities
 Lesion in cortex or subcortical white matter
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Motor Responses
 Decorticate posturing – rigid extension of arms and
legs
• Lesion at brainstem, usually pons
 Flaccid – gravest prognosis with lesion deep in
brainstem
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Management
 ABC’s with neck immobilization if history of trauma
 Bedside glucose
 Hyperventilation to PaCO2 of around 35 mm Hg if
increased ICP suspected
• Increase ventilation until pupils constrict
 Support perfusion
 Neuro exam
• GCS or AVPU
• Pupillary response
• Respiratory pattern
• Treat hypoglycemia with glucose or glucagon IM
• Consider Naloxone
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Management
 Formulate presumptive diagnosis using AEIOU
TIPS
 Pursue specific management
 Admit to PICU:
• Any pt not responding to therapeutic intervention
• Require ongoing monitoring
• Diagnosis in question after initial management
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Prognosis
 In general, pediatric coma patients fare better than
adults
 Predictors of poor outcome
• Long (>25 min) duration of cardiac arrest
• Blood glucose >250
• Unresponsiveness on arrival
• GCS <8 on arrival
• pH < 7.10 on presentation
• Coma > 24 hours
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Trauma
 Epidural Hematoma
• Lens shaped
• Caused by arterial
rupture
• Skull fracture present in
85% of cases
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Trauma
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 Subdural hematoma
• Crescent shaped
• Caused by tearing of bridging veins through dura and
arachnoid
• Skull fracture present in 30% of cases
• Retinal Hemorrhage in 75% of cases
Trauma
 Cerebral Contusion
• Can lead to increased ICP
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Trauma
 Cerebral Edema
• Loss of gray-white
matter interface
• Loss of sulci
• Occurs 12-24 hours
after injury
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Seizure
 All seizures except petit mal are followed by a
post-ictal state
 Measure drug levels for children on
anticonvulsants
 Comatose patients may have non-convulsive
seizures needing an EEG to diagnose
 Assume intracranial lesion with non-immediate
post traumatic seizure or new focal seizure until
proven otherwise
 Fever- consider meningitis, encephalitis, brain
abscess, or febrile seizure
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Meningitis
 Bacterial
• Most common infection
severe enough to cause
profound ALOC
 Non-bacterial
• Slower onset of
symptoms
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Infection
 Brain Abscess
• Chronic sinusitis, chronic
otitis, dental infection,
endocarditis or
uncorrected cyanotic
congenital heart disease
can increase risk
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Encephalitis
 Encephalitis – inflammation of the brain
parenchyma usually due to viral infection
• Mumps and Measles common before
immunization
• Varicella – occurs 2-9 days after rash develops
• Arthropod – varies by geographic areas and
seasonal
• HSV – most common devastating cause
 Death or permanent neurologic damage in
70% of cases
 Affects temporal lobes causing seizures,
parenchymal swelling and uncal herniation
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Tumor
 Tumors
• Can cause seizure,
hemorrhage, increased ICP and
can invade into ARAS
• Ataxia and vomiting, think
infratentorial
• Seizure, hemiparesis, speech or
intellectual problems, think
supratentorial
• Headache, lethargy, vomiting,
think acute hydrocephalus
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Stroke (Cerebrovascular)
 Hemorrhagic is usually due
to aneurysm
• Severe headache
• “Sentinal bleeds” are
common before rupture
• Subarachnoid blood is
seen
 AVM or cavernous
hemangioma
• Low flow and less acute
symptoms
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Stroke (Cerebrovascular)
 Thrombosis or Embolic Stroke
• Occlusion of anterior, middle or posterior cerebral
artery will NOT cause coma
• Carotid infarct can cause coma
• Infarcts eventually lead to increased ICP
• Cerebellar infarcts rarely have coma
• Basilar Artery infarcts cause rapid coma due to
brainstem damage
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Shunts
 Placed for hydrocephalus
 Malfunction due to
mechanical causes or
infection
 Highest risk of failure in first 6
months after surgery
 Intrathecal baclofen pump
overdose can cause coma
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Hypoxia
 Neurons extremely sensitive to hypoxia and cease
function within seconds of hypoxia
 Permanent CNS dysfunction can occur within 4-5
minutes of total anoxia at body temperature
 Hypercarbia can also cause neurologic depression
and coma
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Temperature
 Hypothermia
• Each drop by 1 degree celcius causes a 6% drop
in cerebral blood flow
• 29-31 degrees – delerium, confusion, muscle
rigidity
• 25-29 degrees – comatose, no DTR’s, fixed and
dialated pupils
 Hyperthermia
• Headache, vomiting, seizure, obtundation, or
coma result especially above 41 degrees C
• Infants left in a car exposed to sunlight
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Hypertension
 May lead to cerebral hemorrhage
 Hypertensive encephalopathy
• Usually due to renal, endocrine or cardiac
pathology or toxic ingestion (cocaine)
• Headache, N/V, vision changes, ALOC and coma
can result
• Condition improves once BP has normalized
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Electrolytes
 ALOC may be caused by:
• Abnormality in any cation (Na, Ca, Mg,
Phosphorus)
• Metabolic acidosis or alkalosis
• Hyperammonemia from inborn errors, urea cycle
 Hypoglycemia – most common cause in pediatrics
• Infants and small children have decreased
gluconeogensis
• SBI, Sepsis, dehydration, ethanol or oral
hypoglycemic ingestion are causes
 Hyperglycemia – especially new onset diabetes
have ALOC due to hyperosmolarity
• DKA can lead to cerebral edema
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Psych
 Psychiatric disorders can produce stupor like state
 Psychogenic
• Neuro exam reveals this
 Pt avoids hand falling into face
 Resists eyelid opening
 Increased heart rate to painful stimulus
 Intact neuro exam
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Other Causes
 Renal or Hepatic failure
 Hemolytic Uremic Syndrome can cause coma from
uremia or from basal ganglia infarction
 Reye’s Syndrome
• Antecedent viral illness
• Mitochondrial injury affects all organs
• Severe vomiting followed by combative delirium,
then coma
• Cerebral edema results leading to central
herniation
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Bibliography
 Avner, JR. Altered states of consciousness. Pediatrics in
Review 2006;9:331-338
 Gausche-Hill, M, Fuchs, S, Yamamoto, L. APLS The Pediatric
Emergency Medicine Resource Revised Fourth Edition.
American Academy of Pediatrics and American College of
Emergency Physicians, 2007. p147-153.
 Fleisher, GR, Ludwig, S, Henretig, FM. Textbook of Pediatric
Emergency Medicine Fifth Edition. Lippincott Williams &
Wilkins 2006. p201-212.
 Kanich W, Brady WJ, et al. Altered mental status: evaluation
and etiology in the ED. Am J Emerg Med 2002;20:613-617.
 Meyer PG, Ducrocq S, Carli P. Pediatric neurologic
emergencies. Curr Opin Crit Care. 2001;36:651-659.
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