Evaluation of Altered Mental Status

Kalpesh Patel, MD

Dept. of Pediatric Emergency Medicine

October 25, 2006

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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• 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

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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.