Transcript Evaluation of Altered Mental Status Kalpesh Patel, MD Dept. of Pediatric Emergency Medicine October 25, 2006

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.
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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
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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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