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Evaluation of Altered Mental Status
Kalpesh Patel, MD
Dept. of Pediatric Emergency Medicine
October 25, 2006
2
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.
3
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• http://prohealthsys.com/physical/movies/cranialnerve_n_13.mov
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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
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
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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
37
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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