Pediatric Altered Mental Status
William Mills, Jr., MD, MPH
UNC School of Medicine
Department of Pediatrics
Division of Pediatric Emergency Medicine
Definitions
• Levels of Consciousness
– Consciousness: awareness of one’s self and
environment
– Coma: unresponsive to all stimuli, including pain
Definitions
• Confusion: slowed or impaired cognitive abilities
– Manifested by disorientation, memory deficits, or difficulty following
commands
– Stimuli are misinterpreted and the person is often drowsy
• Delirium: a chain of unconnected ideas such that the patient
appears disoriented, fearful, agitated, and irritable
– Misperception of sensory stimuli can lead to hallucinations
– Usually associated with a toxic/metabolic etiology
• Obtundation: decreased alertness and limited interest in the
environment
– More time is spent sleeping and when awakened, the patient is still
drowsy
• Stupor: responsive only to vigorous, repeated stimuli and
returns to an unresponsive state when left alone
Normal Consciousness
• Normal LOC requires both:
– Awareness
• Determined by the cerebral hemispheres
– Arousal
• Controlled by the ascending reticular activating system
(ARAS)
• Alteration in LOC can be the result of deficits in
awareness, arousal, or both
Anatomic Considerations
• The ARAS is a core brain structure that extends
from the medulla to the thalamus
– Location overlaps several brain stem reflex pathways:
• Pupillary light reflex
• Reflex eye movements that allow conjugate gaze
– Pupillary asymmetry or dysconjugate gaze imply
deficits in the area of the ARAS
– Preservation of these reflexes
• Often means that ARAS function is normal
• Implies that the alteration in mental status is the result of
deficits in both cerebral hemispheres
Common Etiologies of AMS
Structural
Trauma
Intracranial bleed
Cerebral Edema
Shaken baby syndrome
Tumor
Stroke
Hydrocephalus
Medical
Infection
Toxin
Seizure
Metabolic
Intussusception
Hemolytic-uremic syndrome
Psychogenic
Etiology of Altered Level of Consciousness
• Structural etiologies may require operative
intervention
• Most medical etiologies require supportive care
required
• Important to make a rapid assessment of the
likelihood of each of these conditions
– Recognition of an asymmetric neurologic examination
– Systematic assessment of 3 physical exam findings:
• Pupillary response
• Extraocular movements
• Motor response to pain
Pupillary Response
• Presence of the pupillary light reflex may be the most
important sign that differentiates structural from medical
coma
• Sympathetic pathway
– Originate in the hypothalamus, fibers descend to the spinal
cord, preganglionic fibers synapse in the superior cervical
ganglion, and postganglionic fibers travel with the internal
carotid artery into the skull
– Controls pupillary dilatation
• Parasympathetic pathway
– Originate in the midbrain and the postganglionic fibers
accompany the oculomotor nerve
– Controls pupillary constriction
Pupillary Sympathetic and Parasympathetic Pathways
Anatomy of Pupillary Pathways
Pupillary Response
• If damage occurs in:
– Midbrain region
• Parasympathetic pathway is interrupted and pupils will be
slightly enlarged and not responsive to light
– Pontine lesions
• Interfere with the descending sympathetic fibers and result
in small pupils
• Light reflex may be present, but difficult to visualize without
magnification
– 3rd nerve compressive lessions
• Result in a dilated and unresponsive pupil on the same side
as the insult
Pupillary Response
Pupillary Response
• Medical etiologies (especially toxic and
metabolic causes)
– Pupillary response is usually preserved
• May be small, but they are generally symmetric and
reactive
Extraocular Movements
• Areas of the brainstem adjacent to those responsible
for consciousness also mediate oculomotor reflexes
– Conjugate gaze requires preservation of the internuclear
connections of CN III, VI, and VIII via the medial
longitudinal fasciculus (MLF)
• Abducens nerve (through the lateral rectus muscle) moves the
ipsilateral eye laterally and the oculomotor nerve (through the
medial rectus) moves the contralateral eye medially
– Deficits in extraocular movements usually accompany a
structural etiology
• Structural lesions that impinge on these pathways will cause
dysfunction
– Disconjugate gaze
– Opthalmoparesis
Anatomy of Extraocular Movements
Extraocular Movements
• Oculocephalic (Doll’s eyes) reflex
– Elicited by holding the eyelids open and turning the head briskly to each
side
• Normal response is for the eyes to shift left when the head is turned right and
vice versa
• If a low brainstem lesion is present, the eyes will move along with the head
mimicking oculoparesis
• Oculovestibular (Cold caloric) reflex
– Elicited by elevating the head 30 degrees and inserting a small catheter
into the external auditory canal, near the tympanic membrane
– Eyes are held open while 120mL of ice water is flushed into the ear
• Normal response in an unconscious patient is nystagmus with the slow
component toward the ear being irrigated and the fast component away from
the irrigated side (the reverse is true in conscious patients)
• Patients with unilateral MLF lesions will deviate the eye only on the unaffected
side
• Patients with low brainstem lesions will not move either eye in response to this
maneuver
Extraocular Movement Reflexes
Motor Response to Pain
• Decorticate posturing (abnormal flexion)
– Seen with damage to the diencephalon
(uppermost brainstem)
• Decerebrate posturing (abnormal extension)
– Seen with damage to the midbrain and pons
• Flaccid posturing
– Indicates compression of the medulla
– Ominous sign
Motor Response to Pain
Structural Neurologic Derangement
Trauma
• Typical mechanism for accidental or inflicted
trauma:
– Rapid deceleration
• Causes shearing of axons connecting cell bodies (diffuse
axonal injury)
– Shearing of axons that connect the ARAS to higher brain
centers results in loss of consciousness
– Shearing forces can also rupture blood vessels and result in
epidural, subdural, or intraparenchymal hemorrhage
Structural Neurologic Derangement
Tumors
• Generalized effects of tumors that affect level of
consciousness include:
– Seizures, intracranial hypertension due to enlarging mass, or
cerebral edema surrounding the mass
• Primary brain tumors that affect either cerebral hemispheres
or the ARAS of the brainstem may affect the LOC by direct
effect on the neural pathways
• Brainstem and cerebellar tumors are more likely to cause
obstructive hydrocephalus by blocking the third and fourth
ventricles
– Common symptoms include:
• Headache, vomiting, altered mental status, and focal neurologic deficit
• Symptoms may be present for weeks to months before presentation
Structural Neurologic Derangement
Vascular
• Ischemic, thrombotic, or hemorrhagic strokes may cause
AMS by:
– Interfering with cerebral blood flow
– Causing intracranial hypertension secondary to cerebral edema
around the infarction
• The most common cause of hemorrhagic stroke in children
is arteriovenous malformation (AVM)
• Thrombotic and ischemic strokes:
– Most commonly seen in children with sickle cell disease and
congenital heart disease
– Other etiologies include:
• Hypercoagulable states, metabolic disorders (MELAS and
homocystinuria), vasculitis (systemic lupus erythematosis, Henoch
Schonlein purpura, and polyarteritis nodosa), other vascular
abnormalities (Moyamoya, arterial dissection and sinus thrombosis)
Structural Neurologic Derangement
Hydrocephalus
• Hydrocephalus occurs when there is an imbalance between the
production and absorption of CSF
– Causes dilatation of the ventricles and displacement of the cerebral cortex
• Communicating hydrocephalus
– Arachnoid villi are unable to absorb CSF
• Infection, hemorrhage
• Non-communicating hydrocephalus
– Blockage of the normal circulation of CSF
• Congenital malformations, acquired tumors
• Signs and symptoms of shunt obstruction are the same as those for
hydrocephalus
– Proximal obstruction
• Tissue debris, choroid plexus, infection, or migration of the catheter can obstruct the
shunt proximally
– Distal obstruction
• Kinking to the tubing, omentum, infection and migration
4 Types of Brain Herniation
1) Cingulated (subfalcine)
2) Central
3) Uncal (transtentorial)
4) Tonsillar
Progression of Herniation Syndromes
Stage
Mental Status
Pupils
EOMs
Motor Response
Diencephalic (early)
Normal or decreased
Small, reactive
Normal
Appropriate
Diencephalic (late)
Decreased
Small, reactive
Normal
Decorticate
Midbrain, upper pons
Decreased
Midpoint, fixed
Asymmetric
Decerebrate
Lower pons, medulla
Decreased
Pinpoint, fixed
Absent
Flaccid
3rd Nerve (early)
Usually normal
Unilateral, dilated, sluggish
Normal or asymmetric
Appropriate or asymmetric
3rd Nerve (late)
Decreased
Unilateral, dilated, fixed
Asymmetric or absent
Decorticate or decerebrate
Midbrain, upper pons
Decreased
Midpoint, fixed
Asymmetric or absent
Decerebrate
Central
Herniation
Uncal Herniation
Medical Causes of Neurologic Derangement
Infection
• Meningitis
• Encephalitis
• Subdural empyema
– Secondary to meningitis or, more commonly, from direct
extension of paranasal sinus infection or otitis media
– Presentation similar to that of meningitis and seizures occur in
two-thirds of these patients
• Epidural abscess
– Result of contiguous spread of infection from the sinuses or
middle ear
• Sepsis
– Secondary to circulating proinflammatory mediators (cytokines,
endotoxins, etc.) and shock
Medical Causes of Neurologic Derangement
Toxin
• Diagnosis and management of ingestions
dependent on a high index of suspicion
– Many drugs and toxins are not detectable on serum
and urine drug screens
– History is key
– Consider toxidrome
• Clinical “toxin” syndrome characterized by objective data
such as vital signs and clinical features
• 5 general types of toxidromes
–
–
–
–
–
Anticholinergic
Cholinergic
Adrenergic
Opioid
Sedative/hypnotic
Commonly Ingested Agents that Cause AMS
•
•
•
•
•
•
•
Amphetamines
Anticholinergics
Anticonvulsants
Barbiturates
Benzodiazepines
Clonidine
Cocaine
•
•
•
•
•
•
Ethanol
Haloperidol
Narcotics
Phenothiazines
Salicylates
Selective serotonin uptake
inhibitors (SSRIs)
• Tricyclic antidepressants (TCAs)
Medical Causes of Neurologic Derangement
Seizure
• Easily identified as the source of AMS if typical
tonic-clonic movements are witnessed
• Other presentations:
– Post-ictal state
– Subclinical or non-convulsive status epilepticus
– Period of transient paralysis (Todd paralysis)
Medical Causes of Neurologic Derangement
Other
•
•
•
•
•
Hyper- or hypothermia
Hyper- or hypotension
Hypoxia or hypercarbia
Hyper- or hypoglycemia
Abnormal electrolyte concentrations
– Particularly sodium and calcium
• Acute lead toxicity
• Intussusception
– Profound lethargy can be seen, probably due to cytokines released by the
entrapped bowel wall
• Hemolytic-uremic syndrome
– AMS secondary to endothelial damage, platelet activation, and thrombi formation
• IEM
– Secondary to metabolic acidosis, uremia, hyperammonemia, or hypoglycemia
• Psychogenic coma
– Should be considered when all organic causes of coma have been ruled out
Common Diagnoses of Altered Mental Status by Age
Infant
Child
Adolescent
Infection
Toxin
Toxin
Metabolic
Infection
Trauma
Inborn Error of Metabolism
Seizure
Psychiatric
Seizure
Intussusception
Seizure
Abuse
Abuse/Trauma
Mnemonic for Altered Level of Consciousness
AEIOU TIPS
A
E
I
O
U
Alcohol, Abuse of Substances
Epilepsy, Encephalopathy, Electrolyte Abnormalities,
Endocrine Disorders
Insulin, Intussusception
Overdose, Oxygen Deficiency
Uremia
T
I
P
S
Trauma, Temperature Abnormality, Tumor
Infection
Poisoning, Psychiatric Conditions
Shock, Stroke, Space-occupying Lesion (intracranial)
Initial Assessment
• ABCDEs
• Vital Signs
– Temperature
– Cushing Triad
• Hypertension
• Bradycardia
• Abnormal Respirations
Initial Assessment
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•
•
•
•
•
•
•
Pupillary size and reflex
EOM
Motor response to pain
Asymmetry to exam
GCS/AVPU
Smell (alcohol, ketones)
Papilledema
Signs of trauma:
– Bruises, hematomae, hemotympanum, Battle sign, raccoon eyes, and
retinal hemorrhages
• Patients who are feigning unresponsiveness may have:
– Increase in heart rate in response to painful stimuli, resist eye opening,
usually avoid hitting themselves when their hand is allowed to drop to
their face
Initial Assessment
• Respiratory Pattern
– Cheyne-Stokes respiration
• Hyperpnea in a crescendo and decrescendo pattern followed by an apneic phase
• Seen in patients with bilateral hemispheric disease, hypertensive encephalopathy,
conditions which cause cerebral hypoxia, and metabolic conditions
– Central neurogenic hyperventilation
• Sustained, rapid, and deep respiratory pattern that results in a respiratory alkalosis
• May occur with lesions of the midbrain and pons
– Apneustic breathing
• End-inspiratory pauses alternating with end-expiratory pauses
• Consistent with damage to the pons
– Ataxic Breathing
• Completely irregular pattern that may progress to apnea
• Consistent with damage to centers in the medulla responsible for the normal
rhythm of breathing
Management Algorithm for a Child with AMS
Conclusion
6 Pearls of Wisdom
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•
•
•
Assume the worst
Obtain a thorough history
Follow the ABCs and GCS carefully
Fully resuscitate from shock
– Then worry about increased intracranial pressure
• Think about child abuse as the etiology
• Remember to check a blood glucose at
presentation and periodically thereafter