Neurons in the reticular
activating system in the
brainstem and pons
project to the cortex
You need oxygen and
nutrients to stay awake
Normal
AMS
Coma
GCS 15
GCS <15 but >3
GCS 3
• Coma occurs in 30/100,000 children annually
• In nontraumatic coma infection is #1 (38%)
– ½ of these are from N. meningitidis
• Toxic ingestions are #2 (10%)
– But #1 in adolescents (30%)
• Primary CNS Disorders
– Focally affect the brain by exerting external pressure
(bleed/mass) or causing elevated ICP
• Systemic Abnormalities
– Alter neural activity through decreased availability of
substrates (hypotension, oxygen, glucose)
– Altered intracellular metabolism (hypo/hyperthermia)
– Introducing extraneous toxins (ingestions, liver/kidney
failure)
•
•
•
•
•
•
Trauma and hemorrhage
Seizures
Infection
Tumors
Vascular disease (stroke)
Hydrocephalus and CSF Shunt Problems
• Includes blunt trauma/contusions & hemorrhage
Subdural
Epidural
Subarachnoid
Intraparenchymal
• Concussion
– Transient alteration in
normal neurologic function
– Post concussion syndrome
lasts hours-days headache,
nausea, vomiting, dizziness,
lethargy
– Neuroimaging is always
normal
– Grading systems should not
be used in return to play
decisions
• Diffuse cerebral edema
– After trauma, arrest, or
hypoxia
– CT findings may not be
visible for 12-24 hours
• Loss of gray-white
differentiation
• Herniation syndromes
– Transtentorial (uncal): include headache, altered level
of consciousness, followed by bradycardia & pupillary
changes
– Foramen magnum (tonsillar): downbeat nystagmus,
bradycardia, bradypnea, and hypertension ; these
findings may be
• Exacerbated by neck flexion and improved with neck
extension
– Subfalcian (cingulate): unilateral or bilateral weakness,
loss of bladder control, and coma
– Retroalar: hemiplegia, coma, and death due to
compression of the anterior and middle cerebral
arteries
• Unconsciousness occurs during all generalized
seizures, and variably during post ictal period
• Status epilepticus: persistent seizure activity
or intermittent activity without return to
baseline between episodes that last for more
than 5 minutes
• Leads to global CNS dysfunction
– Meningitis
– Encephalitis
– Focal infections (abscess, subdural empyema,
epidural abscess)
Fun Fact: M. pneumoniae, C. pneumoniae and EBV
can cause severe impairment of mental status with or
without meningoencephalitis
• Cause AMS in several ways
– Edema
– Hemorrhage
– Seizure
– Elevated ICP (Obstructive
hydrocephalus)
– Direct invasion of the RAS
• Swelling/bleeding of infarcted brain increases ICP,
thus interrupting blood flow to the RAS
– Infarct
• Thrombotic/Embolic: generally produces focal neurologic
deficit rather than coma
• Hemorrhagic: Rupture of AVM is more likely to result in
coma
– Central venous thrombosis: sequelae of sinusitis or
hypercoagulable states
• Majority of 1st failures due to obstruction
– Shunt over drains
– Ventricles shrink
– Tip gets clogged against choroid plexus
• Median survival of a shunt (before need for revision)
– child under 2 years of age is 2 years
– over two years of age is 8 - 10 years
• Hypoxia
• Cardiovascular abnormalities
– Hypotension
– Arrhythmia
– Hypertensive encephalopathy
• Intoxications
• Metabolic alterations
• Hypo/Hyperthermia
• Permanent CNS dysfunction from anoxia >4-5
minutes
• Etiology
–
–
–
–
Pro Tip:
Airway obstruction or asphyxia
Pulmonary disease
Severe acute anemia/blood loss
Severe methemoglobinemia or CO poisoning
Hypercarbia: cerebral vasodilation
Hypocarbia: cerebral vasoconstriction
• Cerebral blood flow is autoregulated and affected by
numerous factors
• Hypotension
– Poor cerebral perfusion = bad
• Hypertensive Encephalopathy
– Headache, nausea, vomiting, visual disturbance, AMS with BP >95%
for age and gender
– Acute onset suggests renal artery stenosis, glomerulonephritis,
pheochromocytoma, coarctation of the aorta, or cocaine use
• Neuronal function is either directly impaired by the
drugs or through secondary hypoxia, acidosis,
enzyme inhibition, hypoglycemia or seizures
• Select ingestions that cause AMS
– Sedating agents: antihistamines, benzos, barbiturates,
opiates, GHB, ethanol
– TCAs
– Anticonvulsants
– Salicylates
• Neuronal function is either directly impaired by the
drugs or through secondary hypoxia, acidosis,
enzyme inhibition, hypoglycemia or seizures
• Select ingestions that cause AMS
– Sedating agents: antihistamines, benzos, barbiturates,
opiates, GHB, ethanol
– TCAs
– Anticonvulsants
– Salicylates
• Miosis
–
–
–
–
–
–
Narcotics
Clonidine
Organophosphates
GHB
PCP
Ethanol
• Mydriasis
– Anticholinergics (atropine, antihistamines, TCAs)
– Sympathomimetics (amphetamines, caffeine, cocaine, LSD, nicotine)
• Nystagmus
– Barbiturates, ketamine, PCP
• Hypoglycemia is #1
– Sepsis, dehydration, ingestions (ethanol and oral hypoglycemics),
insulin OD
• Metabolic acidosis
– Excess serum cations (Na, Ca, Mg, P) cause AMS
– Severe dehydration alone also causes AMS
• Acute kidney/liver failure
• Reye’s syndrome: acute toxic encephalopathy affecting brain and liver
– Highly unlikely in the face of normal liver enzymes and ammonia
• Urea Cycle Deficits: AMS + hyperammonemia in infants
• Hypothermia
– Each 1oC drop decreases CBF by 6%
– 29-31oC - confusion or delirium
– 25-29oC - comatose with absent DTR
• Hyperthermia
– >41oC headache, vomiting, obtundation
• Intussusception: lethargic as they become
more acidotic
• Hemolytic uremic syndrome: CNS involvement
via infarction (basal ganglia)
• Lupus causes everything
• Unless there is a past history of the exact same behavior it is
dangerous to assume that the cause of AMS is just psych
• Differential of acute psychosis of psychiatric etiology includes
– Schizophrenia and schizophreniform disorder
– Mood disorders
• severe depression: persecutory or self-blaming delusions or
hallucinations
• severe depression or mania in bipolar disorder: grandiose
delusions
– Schizoaffective disorder: schizophrenia + mood disorder
– Brief psychotic disorder
• Acute onset psychosis
– Disruption in thinking, accompanied by delusions or hallucinations
• Delusions: false, fixed beliefs that cannot be resolved through
logical argument
• Hallucinations: false perceptions that have no basis in external
stimuli
– Acute onset occurs more commonly with an underlying medical cause
rather than psychiatric disease
– Even patients with symptoms suggestive of a primary psych diagnosis
should undergo a medical evaluation to exclude possible reversible
etiologies of psychosis
• Patients may feign unconsciousness
– Catatonia is distinguished from coma by the patient's
preserved ability to maintain posture, even to sit or
stand
• ‘Fakers’ usually:
–
–
–
–
Avoid hitting their face with a falling arm
Resist eyelid opening
Raise HR to auditory or painful stimuli
Intact DTR, oculovestibular and oculocephalic reflexes
• Brief hallucinations do occur in the absence of
any organic or psychiatric disease
– Falling asleep and waking
• hypnagogic and hypnopompic hallucinations
– Bereavement: hallucinations of a deceased loved
one are common
– Severe sleep deprivation
– Sensory deprivation and sensory impairment
– Caffeine intoxication
•
•
•
•
•
Epidural hematoma
Cerebral edema
Bain neoplasms
Cerebral infarctions
CSF shunt malfunction
•
•
•
•
•
Meningitis/encephalitis
Toxic ingestions
Hypotension
Hypoxia
Sepsis
• Goal directed questions
– Relevant PMH
– Medications
– Seizures
– Trauma (or if unsupervised
in last 24 hours)
• Progression of known
disease
– DKA
– Congenital heart disease w/
embolic abscess or infarction
• Abrupt and unexplained
onset
–
–
–
–
–
Intracranial hemorrhage
Seizure
Arrhythmia
Trauma
Intoxication
• Gradual deterioration
– Inborn error of metabolism
– Infection
– Mass lesion
• Vague or inconsistent
history from caregiver
– Non accidental trauma
• Vital signs
• AVPU or GCS
• Head trauma signs
– Head lac, skull fracture, hemotympanum , raccoon eyes
• Nuchal rigidity
• Skin: purpuric or varicelliform rashes
• Breathing patterns
– Cheyne-Stokes intervals of waxing and waning
hyperventilation with periods of apnea
– Apneustic: 2-3 second pause with each inspiration
• GCS
– Eye Opening (4)
– Best Motor Response (6)
– Verbal Response (5)
• Alert Voice Pain Unresponsive
• Motor responses and DTRs
Pro Tip: Focal neuro findings are bad
Eye
Opening
Best
Motor
Response
Verbal
Response
Score
4
3
2
1
Older children and adults
6
Obeys commands
Infants and young children
Spontaneous
To Voice
To pain
None
Obeys commands, normal spontaneous
movements for age
Localizes to pain
Normal flexion withdrawal
Abnormal flexion (decorticate)
Extension (decerebrate)
None (flaccid)
5
4
3
2
1
5
Oriented
4
Disoriented, converses
3
Inappropriate words
2
1
Incomprehensible sounds
None
Smiles, oriented to sounds, follows
objects, interacts
Cries but consolable, inappropriate
interactions
Inconsistently consolable and moans,
makes vocal sounds only
Inconsolable restless, agitated
None
• Pupil response is the most direct ‘window to the brain’
– Unilateral enlargement (>5mm) - Herniation
– Bilateral blown (enlarged and unreactive) - Massive CNS
dysfunction (incr ICP)
– Roving conjugate movements metabolic coma
– Persistent conjugate deviation = seizure
– Conditions affecting the brain diffusely spare pupils
• Except for opiates = pinpoint
• Don’t attempt oculocephalic if you suspect trauma or
severely elevated ICP
• Blink then corneal reflex are progressively lost
• Limbs/postural tone
– Light coma: bilateral
restless limb movements
– Decerebrate: midbrain
compression, cerebellar
problems, metabolic
disorders
– Decorticate: cerebral
white matter, internal
capsule, thalamus
• ABC(DE)s
– Airway support
– Oxygen
– IV access
• Vitals are vital
– For instance, in rising ICP vitals change sequentially
• Bradycardia (early sign of herniation in children)
• Hypertension
• Widened pulse pressure
• Cushing’s triad: late finding of brainstem dysfunction
– HTN, bradycardia, irregular respirations
•
•
•
•
•
•
•
Rapid bedside glucose test
Electrolytes including BUN/Cr
Blood gas
CBC
Blood Culture if infection suspected
Liver panel including ammonia
Urine drug screen
•
•
•
•
•
•
Seizure drug levels
Thyroid studies
Coags in sepsis and ICH
Co-Oximetry for CO or MetHgb
Fancy metabolic labs
EKG in ingestions with cardiac effects (TCAs,
BP meds)
• Does every kid with AMS need a head CT?
– All with an acute coma of unknown etiology
should get one
– Also in:
•
•
•
•
•
Signs of elevated ICP
Trauma
Focal findings
Suspected shunt malfunction
Unsupervised child
• Which patients with AMS need an LP?
– Suspected meningitis/encephalitis
– To confirm subarachnoid hemorrhage in a
negative CT
• These patients also need coags in addition to the CT
before they get an LP
– An opening pressure is helpful
• MRI
– Consider in a stroke (after the head CT)
• EEG
– New protocol will allow Neuro to set up EEG in the
ED for status epilepticus
• Trauma and hemorrhage
– Consult Neurosurgery
– Protect airway if GCS ≤8
– Interventions for elevated ICP
•
•
•
•
•
Hypertonic 3% Saline 6-10ml/kg over 5-10 minutes
Mannitol 0.25-1g/kg over 10-20 minutes
Elevate HOB with head midline
Maintain homeostasis (temperature, oxygen, BP etc.)
Don’t hyperventilate unless herniation is imminent
• Seizures
– Postictal patients should improve in 2-3 hours
• Simple febrile seizure generally normal by 1 hour
• If lethargic or irritable >1 hour even after antipyretics be
worried about meningitis/encephalitis
– Focal defects indicate a focal CNS lesion until proven
otherwise
• Get a head CT
– Drug levels, electrolytes
– Empiric Tx for meningitis/encephalitis
– Manage seizures with benzo x2, fosphenytoin then
phenobarb
• Infection
– Antimicrobials as early as possible
– If focal findings or seizure get a head CT to r/o a
focal CNS infection
– CSF analysis
• Pleocytosis in encephalitis is mild (<500 cells/mm3) with
normal glucose and protein
• CSF in HSV encephalitis contains RBC in 50%
• Bloody/xantochromic CSF with elevated opening
pressure, but no pleocytosis suggests SAH
• Tumors
– Consult Onclogy and Neurosurgery
– Interventions to mitigate increased ICP
– Steroids may help – but ask the consultant first
• Vascular disease (stroke)
– Hemorrhagic: Treat seziures and elevated ICP, address
coagulopathy
– Ischemic: supportive care, PICU and Neurology, heparin
• Hydrocephalus and CSF Shunt Problems
– Ask a Neurosurgeon nicely to replace the shunt
• Hypoxia
– Give oxygen
• Cardiovascular abnormalities
– Hypotension: Treat BP to optimize CBF
– Arrhythmia: Heart doctors are helpful here
– Hypertensive encephalopathy: Goal to lower BP by
20% in the first hour, labatelol first, then drip of
labatelol or nicardipine
• Intoxications
– Give Narcan if the patient has miosis or suspected
narcotic (or clonidine) ingestion
– Avoid giving flumazenil to block benzos, as you won’t
be able to treat a subsequent seizure if you give it
– Get urine tox, APAP and ASA, etOH
– EKG in cardioactive meds
• Can toxic ingestions lead to unequal pupils?
– No
• Metabolic alterations
– Treat hypoglycemia
• Neonates D10W 1-2ml/kg IVP (10g/100ml)
• Children D25W 1-4ml/kg IVP (25g/100ml)
• Adults D50W 25g IVP
• Hypo/Hyperthermia
– Raising temperature too quickly can be bad
– <32oC internal and external warming
• Calm and supervised environment
• Mechanical restraints
• Medications
– IM Geodon
• Children 10mg
• Adolescents & Adults 10-20mg
– 69% of 20mg doses exceeded the
calming therapeutic effect
– IM Haldol 2-5mg q4-8 hrs
• Give with IM Cogentin 1mg
– PO/IV Ativan 0.05 mg/kg/dose - max 2mg
• PO effective within 30 minutes
• Stabilize patient (ABCs) get IV and test at least rapid
glucose (consider ISTAT)
• Unless you are absolutely sure that the cause is
extracranial get a head CT
– Mass lesion, bleed, ventricle size, intracranial HTN
• Await other labs and prepare for LP
– Measure opening pressure
ABCDE
+ Bedside glucose +
Supplemental O2
Fluids
Cooling/warming
Labs + correct aberrant glucose/lytes
Antibiotics if any suspicion of infection
Head CT
LP
Neuro Consult
IV
• Assuming no head trauma occurred in the absence of
corroborating history
• Neglecting to secure the airway before getting a head CT
• Hyperventilating an intubated patient to a pCO2 well below
35 mmHg
• Not sedating the paralyzed/intubated patient
• Believing that a toxic ingestion has not occurred just
because the urine drug screen is negative
• 7yo F with acute onset AMS
– Woke up normally, then went back to bed shortly
thereafter
– Upon reawakening she was confused and disoriented
– 2d ago ‘low grade fever’ and headache
– Yesterday NBNB emesis x3
• Normal PMH, vaccines UTD, no recent shots
• No ingestions, no trauma
AMS in triage – Medical Team called
VS: T 38.7 HR 140 RR 25 BP 92/58
GEN: confused
HEENT: NCAT, EOMI, PERRLA, TM wnl, sweet smelling breath
NECK: no LAN, patient winced when head passively moved
CV: tachycardic, no murmur, 3-4 sec cap refill, 2+ peripheral
pulses
PULM: CTAB, no wheezes or crackles
GI: soft, NTND, no masses, no HSM
SKIN: no rashes
NEURO: MAEW, GCS 13 (-1 V & -1 E)
What are your top 3 diagnoses?
What do you want to do?
ISTAT: 7.54/28/+1, Glucose 186, HCO3 24, Na 133
Urine 3-4 wbc/hpf, LE and NIT negative
Liver, ammonia normal
Renal with Na 134
CBC wbc 34 86% segs H/H 11.7/35.2 Plts 520
Utox ASA and Acet negative
CXR normal
Head CT mild diffuse cerebral swelling, no herniation or acute
hemorrhage
• LP
–
–
–
–
Glucose <20
Protein 433 mg/dL
RBC 642 WBC 1266
Gram stain: WBCs and gram + cocci in pairs and chains
• Diagnosis
– Bacterial meningitis
– Started ceftriaxone and vancomycin
– Admitted to PICU
– Ultimately grew S. pneumo in CSF, but B/C negative
• 12 yo M fell backwards off a diving board
ladder 4-5 feet onto concrete
– Questionable LOC, now tearful and very anxious
– EMS: C collar and backboard
• PMH: neck injury about 6 weeks ago when he
ran into some bleachers. In a ‘neck brace’ due
to that injury for a short time
Trauma eval
VS: T 37.2 HR 63 RR 29 BP 132/63 SAT 100%
GEN: WDWN, tearful, anxious confused
HEENT: 1-2 inch area of soft tissue swelling over right occiput.
No laceration. PERRLA, EOMI, TM wnl, mmm
NECK: Negative for midline C spine pain
CV: RRR, nl S1 and S2, 2+ pulses, 2 sec cap refill
PULM: CTAB
GI: soft, NTND, no masses, no HSM
SKIN: no rashes
NEURO: MAEW, GCS 14 (-1 V)
According to the latest head injury guidelines
should this child get a head CT?
• Absolutely!
– LOC + GCS 14
– There is a Head Injury Tool in Epic that can help
assess these risk factors
• https://vimeo.com/36792246
Hemorrhage into a pre-existing temporal
lobe arachnoid cyst
• Ultimately admitted to PICU after
Neurosurgical consultation
• No emergent surgery
• Subsequent Neuroimaging stable
• Other than occasional headaches he has done
quite well
• 21mo F w/ sickle cell disease
• 1d of fever at home and 2d of mild URI Sx
• No vomiting, diarrhea, cough or difficult
breathing
• Developed progressive lethargy throughout
the evening
Medical Team
VS: T 38.6 HR 154 RR 34 BP 90/56 SAT 96% RA
GEN: lethargic, responds to painful stim, cries for mommy
HEENT: NCAT, PERRLA, EOMI, TM wnl, mmm
CV: tachycardic, nl S1 and S2, 1+ peripheral pulses, 2+ central
pulses, 5 sec cap refill
PULM: CTAB but grunting
GI: distended, non tender, spleen tip palpable 4cm below LCM
SKIN: pale and sallow, no rashes
NEURO: MAEW, GCS 13 (-1 M -1E)
What complication of sickle cell are you worried about?
What do you want to do?
Multiple pIV attempts unsuccessful so IO placed in R
proximal tibia
ISTAT: 7.22/44/-9, Glucose 168, HCO3 18.5, H/H 3.1/10
CXR no focal disease
• Over the next 30min lethargy progressed and perfusion
worsened
– She had received 40ml/kg NS and Rocephin
• Labs came back
– CBC wbc 27 60% segs H/H 3.3/9.3 Plts 61
– PTT 64.8 PT 25.5 INR 2.18
– Renal unremarkable, aside from glucose 151
• Eventually she was noted to have extensor posturing
with eyes deviated to left
– Ativan given, which abated the seizure
• With progressive decline in MS we intubated
via RSI
• Though T&S not available she got 5ml/kg O- pRBC
• Head CT showed no hemorrhage or mass effect, no
edema
• Admitted to PICU with the dual diagnoses of…
– Splenic sequestration and Sepsis
• 6 y/o M brought to ED by aunt for confusion
and AMS
• He was fine until after dinner
• Acting ‘weird’ and picking at ‘bugs’ in the air
• No PMH, no meds or allergies
• He was at the aunt’s house all day long
– Being watched by the aunt and his 13 y/o cousin
Evaluated in the D Pod
VS: T 37.0 HR 146 RR 18 BP 112/62 SAT 100% RA
GEN: alert, confused, making repeated pinching motions in air and on
clothes, diaphoretic
HEENT: NCAT, pupils symmetrically dilated (8mm) and reactive, EOMI, TM
wnl, mmm
CV: tachycardic, nl S1 and S2, 2+ pulses, nl perfusion
PULM: CTAB
GI: normal
SKIN: normal
NEURO: MAEW, nonfocal motor and sensory, answers questions
somewhat appropriately (knows his name, and where he is), seems
confused
What toxindrome is this consistent with?
What do you want to do?
•
•
•
•
EKG NSR
Renal normal
APAP and ASA normal
Utox + for amphetamines
• Oh, and by the way, his aunt later volunteered
that her daughter (the patient’s erstwhile
babysitter cousin) has ADHD
• The patient was later found to have ingested an
unknown amount of her Ritalin
– Admitted to telemetry and ultimately his mental
status and VS normalized
• Ironically he was also diagnosed with scabies…
Take home points about patients with Altered Mental Status
1. Altered mental status is caused by an underlying disease
process
2. Always check glucose
3. If you can’t exclude an intracranial process, or the child was
recently unsupervised get a head CT
4. Do an LP if you don’t have another cause after CT, and to
evaluate for infection, or if you suspect SAH
5. Even with a past history of mental health illness acute onset
psychosis is more commonly associated with an underlying
medical cause