Altered mental status is a sign of serious

neurologic or systemic disease. The

physician must rapidly assess the depth
of coma and risk of intracranial
hypertension, then determine the
etiology and prescribe appropriate
management. This is no small task,
considering the variety and multitude of
illnesses that may present with altered
mental status. The etiologies can be
broken down into structural and medical
causes. The structural causes more
frequently affect the brainstem centers
adjacent to the ascending reticular
activating system that are responsible for
pupillary response and oculocephalic
reflexes. Medical causes generally spare
these structures. Management of
Altered Mental Status
structural lesions requires prompt
diagnosis and neurosurgical input.
Medical etiologies are protean and
treatment is often supportive.
Clin Ped Emerg Med 4:171-178. By Diana King, MD, and Jeffrey R. Avner, MD
© 2003 Elsevier Inc. All rights reserved.
BRONX, NEW YORK

C
ONSCIOUSNESS IS GENERALLY THOUGHT OF as aware-
ness of one’s self and environment while coma is unrespon-
siveness, even to a painful stimulus. However, between the
conditions of consciousness and coma, there are several
states with definitions that are often misused, including confu-
sion, delirium, obtundation, and stupor. A confused person has
slowed or impaired cognitive abilities manifested by disorienta-
tion, memory deficits, or difficulty following commands. Stimuli
are misinterpreted and the person is often drowsy. Delirium is a
chain of unconnected ideas such that the patient appears disori-
ented, fearful, agitated, and irritable. Misperception of sensory
stimuli can lead to hallucinations. This state is usually associated
with a toxic/metabolic etiology. Obtundation is decreased alert-
ness and limited interest in the environment. More time is spent
sleeping and when awakened, the patient is still drowsy. In
stupor, the patient is responsive only to vigorous, repeated stim-
uli and returns to an unresponsive state when left alone.1 Al-
though each of the above terms connote a specific altered state,
the clinician should appreciate that they are quite often misused
and can therefore lead to poor communication between health
care providers. For this reason the Glasgow Coma Scale (GSC) is
often a much more reliable means of conveying the level of
consciousness in a patient.

From the Division of Pediatric Clinical Assessment

Emergency Medicine, Department of
Pediatrics, Children’s Hospital at
Montefiore, Albert Einstein College of
Medicine, Bronx, NY.
Address reprint requests to Diana King,
MD, Pediatric Emergency Medicine,
Children’s Hospital at Montefiore, 111
East 210th Street, Bronx, NY 10467.
E-mail: Dking@montefiore.org
© 2003 Elsevier Inc. All rights
reserved.
1522-8401/03/0403-0000$30.00/0
doi:10.1016/S1522-8401(03)00058-2
Normal consciousness requires both awareness and arousal.
Awareness is the combination of cognition and affect that can be
inferred based on the patient’s interaction with the environment.
Thus, alterations of consciousness may be the result of deficits in
awareness, arousal, or both. Awareness is determined by the
cerebral hemispheres whereas arousal is controlled by the as-
cending reticular activating system (ARAS) commonly called the
sleep center. A helpful analogy is a bulb-switch model where the
cerebral hemispheres function as a light bulb and the ARAS

A LTERED MEN TA L STA TUS / K I N G A N D A V N ER 171

172 A LTE R ED M ENT A L S T A T U S / K ING A ND A VN ER
functions as a light switch. Normal consciousness
requires the light bulb to be lit; to do so requires
both the bulb and the switch to function properly. If
the bulb is “out,” there can either be a problem
with the bulb itself, the switch, or both. Similarly,
altered mental status can result from depression of
both cerebral hemispheres, localized abnormality
of the sleep center, or global central nervous system
dysfunction.1 Components necessary for the bulb
to function are relative normothermia and blood
flow, delivery of energy substrates (oxygen and glu-
cose), and absence of toxins (metabolic waste prod-
ucts, poisons, and infectious material).2
The ARAS is a core brain structure that courses
from the medulla to the thalamus. Serendipitously,
the ARAS’ location overlaps several brain stem re-
flex pathways, in particular those responsible for
the pupillary light reflex and the reflex eye move-
ments that allow conjugate gaze. Thus, preservation
of these reflexes often means that ARAS function is
normal and therefore implies that the alteration in
mental status is the result of deficits in both cere-
bral hemispheres. Conversely, pupillary asymmetry
or dysconjugate gaze imply deficits in the area of
the ARAS.1
It is often helpful to divide the etiologies of al-
tered mental status into 2 groups: structural and
medical (toxic-infectious-metabolic) (Table 1).
Structural etiologies usually cause compression or
dysfunction in the area of the ARAS whereas most
medical etiologies lead to general dysfunction of
both cerebral hemispheres. Common etiologies ac-
cording to age are presented in Table 2. Since struc-
tural etiologies may require operative intervention
as opposed to the supportive care required for most
medical etiologies, it is important for the emer-
gency physician to make a rapid assessment of
the likelihood of each of these conditions. This
TABLE 1. Common Etiologies of Altered
Mental Status
Structural Medical
Trauma Infection
Intracranial bleed Toxin
Cerebral edema Seizure
Shaken baby syndrome Metabolic
Tumor Intussusception
Stroke Hemolytic-uremic syndrome
Hydrocephalus Psychogenic
TABLE 2. Common Diagnoses of Altered Mental
Status by Age
Infant Child Adolescent
Infection Toxin Toxin
Metabolic Infection Trauma
Inborn Error Seizure Psychiatric
Seizure Intussusception Seizure
Abuse Abuse/Trauma
can be done through the recognition of an asym-
metric neurologic examination and the system-
atic assessment of 3 physical exam findings:
pupillary response, extraocular movements, and
motor response to pain.
Pupillary Response
The areas of the brainstem that control con-
sciousness and pupillary response are anatomically
adjacent. The sympathetic and parasympathetic
nervous systems control pupillary dilatation and
constriction, respectively. The sympathetic path-
way originates 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. The parasympathetic pathway originates in
the midbrain and the postganglionic fibers accom-
pany the oculomotor nerve. Knowledge of these
pathways helps localize where a lesion may be
based upon pupillary signs. If damage occurs in the
midbrain region, the 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. The light reflex may be present, but
difficult to visualize without magnification. Lesions
that compress the third nerve will result in a dilated
and unresponsive pupil on the same side as the
insult.
Pupillary response is usually preserved when al-
tered mental status is secondary to medical etiologies
(especially toxic and metabolic causes). The pupils
may be small, but they are generally symmetric and
reactive. Therefore, the presence of the pupillary light
reflex may be the most important sign that differen-
tiates structural from medical coma.1

Extraocular Movements
Areas of the brainstem adjacent to those respon-
sible for consciousness also mediate oculomotor
reflexes. The ability to maintain conjugate gaze
requires preservation of the internuclear connec-
tions of cranial nerves 3, 6, and 8 via the medial
longitudinal fasciculus (MLF). For example, propri-
oceptive inputs from cervical muscles (eg, when the
head is turned to a side) ascend through the MLF in
the brainstem to reach the ipsilateral abducens nu-
cleus. The stimulus then crosses and continues to
ascend through the MLF to reach the contralateral
oculomotor nucleus. These pathways, therefore, al-
low for the coordination of the ipsilateral abducens
and contralateral oculomotor nerves. The 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; hence, there is conjugate gaze. As
with pupillary responses, structural lesions that im-
pinge on these pathways will cause dysfunction
ranging from disconjugate gaze to opthalmoparesis.
Therefore, deficits in extraocular movements usu-
ally accompany a structural etiology.
There are several reflexes that can test extraoc-
ular function in an unconscious patient. The ocu-
locephalic (Doll’s eyes) reflex is 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.
This reflex should not be performed in a patient
with suspected spinal cord injury. The oculoves-
tibular reflex (cold caloric) is elicited by elevating
the head 30 degrees and inserting a small catheter
into the external auditory canal, near the tympanic
membrane. The eyes are held open while 120cc of
ice water is flushed into the ear. The normal re-
sponse 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 while those with low
brainstem lesions will not move either eye in re-
sponse to this maneuver.1
Motor Response to Pain
Abnormal motor movements may also help pin-
point the location of a lesion. Decorticate posturing
(abnormal flexion) can be seen with damage to the
A LTERED MEN TA L STA TUS / K I N G A N D A V N ER 173
diencephalon (uppermost brainstem). Decerebrate
posturing (abnormal extension) can be seen with
damage to the midbrain and pons. Flaccid posturing
is an ominous sign and indicates compression of the
medulla, a terminal event.1
In summary, structural causes will often lead to
compression or dysfunction of the brain stem and
therefore present with pupillary abnormality (un-
equal, unreactive, or sluggishly reactive) and focal
neurologic findings. Medical causes usually result
from involvement of both cerebral hemispheres;
the pupils are generally equal and reactive (al-
though the reaction may be sluggish) and the neu-
rologic examination is non-focal. There are,
however, some notable exceptions. Structural dis-
orders without focality include acute bilateral cere-
brovascular disease and early acute hydrocephalus.
Medical encephalopathies with focality include hy-
perglycemia, hypoglycemia, hypercalcemia, he-
patic encephalopathy, uremia, and some toxic
ingestions.
Etiologies
A complete list of conditions that may present
with altered level of consciousness is not practical.
We will therefore discuss only the major categories
with the most common illnesses.
Structural Neurologic Derangement
Trauma
The typical mechanism for accidental or in-
flicted trauma is rapid deceleration that causes
shearing of axons connecting cell bodies (diffuse
axonal injury). The shearing of axons that connect
the ARAS to higher brain centers results in loss of
consciousness. Contusions are most common in the
frontal and temporal regions. The shearing forces
can also rupture blood vessels and result in epi-
dural, subdural, or intraparenchymal hemorrhage.
Subdural and epidural hematomas may require
emergent evacuation. The role of the emergency
physician is centered on preventing secondary in-
juries that occur due to hypoxia, ischemia, hypo-
tension, seizures, and cerebral edema.3 The
Glasgow Coma Scale is a helpful measure of sever-
ity of head injury, and intubation and controlled
hyperventilation is the standard of care for a score
of 8 or less.4
174 A LTE R ED M ENT A L S T A T U S / K ING A ND A VN ER
Tumors
Primary brain tumors that affect either cerebral
hemispheres or the ARAS of the brainstem may
affect the level of consciousness by direct effect on
the neural pathways. Generalized effects of tumors
that affect level of consciousness include seizures,
intracranial hypertension due to enlarging mass, or
cerebral edema surrounding the mass. Brainstem
and cerebellar tumors are more likely to cause ob-
structive hydrocephalus by blocking the third and
fourth ventricles. Symptoms may be present for
weeks to months before presentation. Common
symptoms include headache, vomiting, altered
mental status, and focal neurologic deficit.5
Vascular
Ischemic, thrombotic, or hemorrhagic strokes
may cause altered mental status by interfering with
cerebral blood flow and by causing intracranial hy-
pertension secondary to cerebral edema around the
infarction. Hemorrhagic and ischemic strokes oc-
cur with the same frequency in children. The most
common cause of hemorrhagic stroke in children is
arteriovenous malformation (AVM).6 Thrombotic
and ischemic strokes are most commonly seen in
children with sickle cell disease and congenital
heart disease. Other etiologies include hypercoag-
ulable states, metabolic disorders (MELAS and
homocystinuria), vasculitis (systemic lupus erythe-
matosis, Henoch Schonlein purpura, and poly-
arteritis nodosa), and other vascular abnormalities
(Moyamoya, arterial dissection and sinus thrombo-
sis).7 Ischemic strokes present with focal deficits
and hemorrhagic strokes present with altered men-
tal status and headache.6
Hydrocephalus
Hydrocephalus occurs when there is an imbal-
ance between the production and absorption of
cerebrospinal fluid (CSF). This causes dilatation of
the ventricles and displacement of the cerebral cor-
tex. Communicating hydrocephalus occurs when
the arachnoid villi are unable to absorb CSF nor-
mally due to infection or hemorrhage. Noncommu-
nicating hydrocephalus occurs when there is a
blockage of the normal circulation of CSF, usually
due to congenital malformations or acquired tu-
mors. Infants present with head enlargement, thin
scalp with distended veins, and full or bulging fon-
tanel. They may have irritability, vomiting, and
poor feeding. “Setting sun” sign may be seen, which
is created by weakness of cranial nerve VI, resulting
in decreased upward gaze. Once the fontanels have
closed the typical symptoms are headache, nausea,
and vomiting. As intracranial pressure rises, pa-
tients become lethargic and may have increased
muscle tone and posturing.8 The treatment of hy-
drocephalus requires diverting CSF via a shunt sys-
tem. The ventriculoperitoneal shunt is most
common. Tissue debris, choroid plexus, infection,
or migration of the catheter can obstruct the shunt
proximally. Distal obstruction results from kinking,
omentum, infection and migration. The signs and
symptoms of shunt obstruction are the same as
those for hydrocephalus.9
Medical Causes of Neurologic Derangement
Any process that decreases or interferes with the
delivery or utilization of substrate to the brain can
alter brain activity. Hyper- or hypothermia, hyper-
or hypotension, hyper- or hypoglycemia, hypoxia,
and hypercarbia can all result in altered conscious-
ness. Abnormal electrolyte concentrations (partic-
ularly sodium and calcium) can lead to seizures and
coma. Build-up of waste products due to renal or
hepatic failure can also alter the level of conscious-
ness.
Infections
Central nervous system infections can rapidly
progress to coma and death. Fever, irritability,
vomiting, and lethargy often accompany meningi-
tis. Headache and neck stiffness are manifested in
children older than two years of age.10 Subdural
empyema can occur secondary to meningitis or,
more commonly, from direct extension of paranasal
sinus infection or otitis media. Infection can extend
to both hemispheres. The presentation is similar to
that of meningitis and seizures occur in two-thirds
of these patients.11 Mortality is higher in patients
who present in coma.12 Older children and adoles-
cents can develop an epidural abscess as a result of
contiguous spread of infection from the sinuses or
middle ear. Patients do not come to attention until
focal neurologic deficits or seizures ensue.11 Sepsis
can also cause depressed mental status secondary
to circulating proinflammatory mediators (cyto-
kines, endotoxins, etc) and shock.
Toxins
Accidental and intentional ingestions of drugs
and toxins are a common pediatric occurrence.
Many ingestions present with altered mental status

TABLE 3. Ingestions Associated With Coma
Amphetamines
Anticholinergics
Barbiturates
Benzodiazepines
Carbamazepine
Carbon monoxide
Clonidine
Cocaine
Ethanol
Gamma hydroxybutyrate (GHB)
Haloperidol
Narcotics
Phencyclidine (PCP)
Phenothiazines
Phenytoin
Salicylates
Selective serotonin reuptake inhibitors (SSRIs)
Tricyclic antidepressants
(Table 3). Diagnosis and management of ingestions
is dependent on a high index of suspicion, as many
drugs and toxins are not detectable on serum and
urine drug screens.13 There has been a recent in-
crease in the number of children on psychotropic
medications; therefore, an awareness of their ad-
verse effects is important. The “serotonin syn-
drome” results from toxicity due to selective
serotonin reuptake inhibitors, usually occurring af-
ter an increase in the dose. The neuromuscular
manifestations are myoclonus, muscle rigidity, and
hyperreflexia; the neurobehavioral signs are rest-
lessness, seizures, coma; and the autonomic signs
are hyperthermia, hypo- or hypertension, and
tachypnea.14,15
Seizures
Convulsions are easily identified as the source of
altered mental status if typical tonic-clonic move-
ments are witnessed. However, children may also
present in a post-ictal state, without a clear history
of a seizure, thus making the diagnosis more diffi-
cult to determine. Furthermore, seizures may be
followed by a period of transient paralysis (Todd’s
paralysis) that is often present on 1 side of the
A LTERED MEN TA L STA TUS / K I N G A N D A V N ER 175
body. This may lead the clinician to suspect a struc-
tural etiology rather than seizure. Nonconvulsive
status epilepticus should be considered in comatose
children without signs of seizure activity. An EEG
will help to diagnose this condition.16
Other Medical Etiologies
The classic presentation of intussusception is
intermittent abdominal pain, vomiting, and currant
jelly stools in children 3 to 9 months of age. Pro-
found lethargy can also be seen, probably due to
cytokines released by the entrapped bowel wall.
Occasionally, there is no history of abdominal com-
plaints and lethargy is the presenting symptom.
Inflamed Peyer’s patches secondary to viral infec-
tion are thought to be the lead point in most
cases.17 It is also important to note that intussus-
ception is occurring more frequently in children
older than 2 years of age.18 Hemolytic-uremic syn-
drome secondary to E. coli O157:H7 can also cause
altered mental status secondary to endothelial
damage, platelet activation, and thrombi formation.
The central nervous system is frequently involved,
with symptoms including lethargy, seizures, and
coma. Cerebral infarcts may also occur.19 Children
with inborn errors of metabolism (eg, urea cycle
defects, organic acidurias) may present with leth-
argy and altered mental status secondary to meta-
bolic acidosis, uremia, hyperammonemia, or
hypoglycemia. Acute lead toxicity can present with
lethargy or irritability accompanied by abdominal
pain, anorexia, pallor, ataxia, or seizure. Finally,
child abuse due to shaken impact syndrome should
be considered in any infant with altered mental
status, especially if there is a vague history of
trauma, associated bruising, or other characteristic
clinical signs.
When all organic causes of coma have been ruled
out, the diagnosis of psychogenic coma should be
considered.
General Approach
Initial Assessment
Airway, breathing, circulation, and dextrose de-
termination (ABCD) are always the first concern
when faced with a patient with altered level of
consciousness. Vital signs will indicate if there is
derangement in temperature control, heart rate,
respiratory rate and pattern, and blood pressure.
Hypoglycemia is readily detected by bedside deter-
mination within a few minutes. Once the patient is
176 A LTE R ED M ENT A L S T A T U S / K ING A ND A VN ER
stabilized, a focused history should be obtained.
Important features of the history include the cir-
cumstances of the onset of the neurologic symp-
toms (eg, gradual or abrupt onset), preceding
neurologic symptoms (weakness, headache, sei-
zure, dizziness, diplopia, vomiting), trauma (wit-
nessed or suspected), drug use or access to drugs,
bloody stools (hemolytic uremic syndrome or in-
tussusception), and whether the history is incon-
sistent with the injury noted (child abuse).
Contributing past medical history may include
brain tumor, VP shunt, seizure disorder, sickle cell
disease, metabolic disorder, diabetes, renal failure,
and liver disease. Physical examination will help
differentiate structural neurologic injury from a
systemic abnormality. Rapid recognition of intra-
cranial hypertension is crucial.
Intracranial Hypertension
There are 3 components within the cranium:
brain, cerebrospinal fluid, and blood. When there is
an increase in the volume of any of these compo-
nents, the intracranial pressure (ICP) will increase.
Elevated intracranial pressure can cause hernia-
tion, which may result in irreversible brain damage
or death. A history of severe headaches (especially
those that improve with elevation), vomiting, visual
changes, and altered behavior or level of conscious-
ness may indicate elevated ICP. Physical signs that
may point to increased ICP include papilledema,
cranial nerve palsies, abnormal mental status, and
posturing. The ominous Cushing’s triad (bradycar-
dia, hypertension, and irregular respirations) is a
sign of impending herniation.8
Physical Examination
A thorough physical and neurologic evaluation
should be performed. Assessment of the patient’s
level of conscious as well as frequent reassessment
of the mental status is crucial in following the
course of illness. As reviewed earlier, pupillary size
(normal or asymmetric) and reflex (fixed or reac-
tive), extraocular movements (normal, asymmetric
or absent), and motor response to pain (normal,
decorticate, decerebrate, or flaccid) are important
clues to determining whether the etiology of the
illness is structural or medical. Assymetry to the
examination also points towards a structural lesion.
The GSC score can also be helpful in assessing the
depth of coma in patients with head trauma. A
score of 8 or less indicates severe injury.20
Identifying abnormal respiratory patterns can
also assist in differentiating a structural neurologic
condition from a medical condition. Cheyne-Stokes
respiration is characterized by hyperpnea in a cre-
scendo and decrescendo pattern followed by an
apneic phase. It is seen in patients with bilateral
hemispheric disease, hypertensive encephalopa-
thy, conditions which cause cerebral hypoxia, and
metabolic conditions. Central neurogenic hyper-
ventilation may occur with lesions of the midbrain
and pons. It is a sustained, rapid, and deep respira-
tory pattern that results in a respiratory alkalosis.
Apneustic breathing consists of end-inspiratory
pauses alternating with end-expiratory pauses. This
pattern is consistent with damage to the pons. Re-
spiratory centers in the medulla are responsible for
the normal rhythm of breathing. Damage at this
level produces ataxic breathing, which is a com-
pletely irregular pattern that may progress to ap-
nea.1
The physical exam should include a search for
signs of trauma: bruises, hematomas, hemotympa-
num, Battle’s sign, raccoon eyes, and retinal hem-
orrhages. The breath may indicate alcohol use or
diabetic ketoacidosis. Patients who are feigning un-
responsiveness will have an increase in heart rate
in response to painful stimuli, may resist eye open-
ing, and usually avoid hitting themselves when
their hand is allowed to drop to their face.
Management
A management algorithm is shown in Figure 1.
The patient should be placed on a cardiorespiratory
monitor and a pulse oximeter. Oxygen should be
routinely administered. If the patient has an unsta-
ble airway, abnormal breathing pattern, or a GCS of
8 or less, rapid sequence intubation should be per-
formed with a attention to cerebral protection. In-
travenous (IV) access should be obtained and blood
drawn for laboratory studies and a bedside blood
glucose level. Fluid boluses should be given if hy-
potension or poor perfusion are noted, and dextrose
given for hypoglycemia. Hypertensive crisis should
be treated with antihypertensives, but hyperten-
sion in a patient with increased ICP may be an
appropriate physiologic response for maintaining
cerebral perfusion pressure.
Patients with traumatic injuries or structural ab-
normalities and signs of increased ICP should have
an emergent head computed tomography (CT) and
neurosurgical consult. They should be mechani-
cally ventilated to a pCO2 of 35, and given IV
mannitol (1g/kg). The cerebral perfusion pressure
(CPP) is the mean arterial pressure (MAP)–ICP, and
a minimum of 70 mmHg is the goal of therapy.
Neurosurgery may place a ventriculostomy, which

Figure 1. Management algorithm for a child with altered mental status.
serves to measure ICP and drain CSF (which re-
duces ICP).20 Obstructive hydrocephalus from tu-
mor or obstructed shunt may need to be relieved
emergently via VP shunt tap or ventriculostomy.9
Patients with new-onset seizures may warrant a
head CT, especially if the seizures are focal. Pa-
tients with known seizure disorder should have an-
ticonvulsant levels checked.
Infants under the age of 1 year who present with
a change in mental status, seizures, apnea, or pos-
turing may have suffered non-accidental trauma. A
head CT should be performed and fundoscopy may
reveal retinal hemorrhages. Coagulation profile and
liver function tests should be sent as coagulopathy
may be associated with brain injury and elevated
transaminases may indicate occult intraabdominal
A LTERED MEN TA L STA TUS / K I N G A N D A V N ER 177
trauma. The goal of management is to maintain
CPP.21
Consider giving activated charcoal if ingestion is
suspected; a cuffed endotracheal tube may be re-
quired in patients with obtundation or decreased
gag reflex to prevent aspiration. Adolescents fre-
quently ingest multiple substances and an electro-
cardiogram should be performed to detect any
changes in conduction intervals. Naloxone can be
given if narcotic overdose is suspected.13
Patients with fever should be given intravenous
antibiotics. A lumbar puncture should be per-
formed, but only if the child is hemodynamically
stable, has no sign of increased intracranial pres-
sure, and has a maintainable airway. Antibiotic ad-
ministration should be prompt regardless if the
178 A LTE R ED MENT A L S T A T U S / K ING A ND A V N ER
lumbar puncture is delayed or deferred. Any focal-
ity to the exam warrants a CT scan; finding empy-
ema or abscess with mass effect contraindicates
lumbar puncture and emergent neurosurgical con-
sultation is indicated.
Blood sent for blood gas, chemistries, and liver
function might reveal acid-base and electrolyte dis-
turbances as well as renal and hepatic dysfunction.
Ammonia and coagulation profile assist in diagnos-
ing hepatic encephalopathy.
Guaiac-positive stools may indicate intussuscep-
tion and abdominal sonogram is an excellent
screening tool. If intussusception is suspected, air
contrast enema is the first treatment modality uti-
lized. If the enema is unsuccessful in reducing the
intussusception, laparotomy with manual reduc-
tion is required.17
Summary
When presented with a patient with altered level
of consciousness, the goal of the emergency physi-
cian is to stabilize vital functions, perform diagnos-
tic tests that will clarify the etiology, and dictate
management. The rapid recognition of intracranial
hypertension is essential and access to neurosurgi-
cal consultation may be life-saving. Patients should
be transferred to a critical care setting until they
return to a normal level of consciousness.
References
1. Plum F, Posner J: The Diagnosis of Stupor and
Coma. Philadelphia, PA, FA Davis, 1980.
2. Adams RD, Victor M, Ropper AH (eds): Principles
of Neurology (ed 6). New York, NY, McGraw-Hill, 1997.
3. Johnston MV, Gerring JP: Head trauma and its
sequelae. Pediatr Ann 21:362-368, 1992.
4. Meyer PG, Ducrocq S, Carli P: Pediatric neuro-
logic emergencies. Curr Opin Crit Care 7:81-87, 2001.
5. Snyder H, Robinson K, Shah D, et al: Signs and
symptoms of patients with brain tumors presenting to the
emergency department. J Emerg Med 11:253-258, 1993.
6. Earley CJ, Kittner SJ, Feeser BR, et al: Stroke in
children and sickle cell disease: Baltimore Washington co-
operative young stroke study. Neurology 51:169-176, 1998.
7. Carlin TM, Chanmugam A: Stroke in children.
Emerg Med Clin North Am 20:671-685, 2002.
8. Pattisapu JV: Etiology and clinical course of hy-
drocephalus. Neurosurg Clin North Am 36:651-659,
2001.
9. Key CB, Roghrock SG, Falk JL: Cerebrospinal
fluid shunt complications: An emergency medicine per-
spective. Pediatr Emerg Care 11:265-273, 1995.
10. Fleisher GR: Infectious disease emergencies, In:
Fleisher GR, Ludwig S (eds): Textbook of Pediatric Emer-
gency Medicine (ed 4). New York, Lippincott Williams
and Wilkins, 2000, pp. 725-793.
11. Bockova J, Rigamoniti D: Intracranial empyema.
Pediatr Infect Dis J 19:735-737, 2000.
12. Krauss WE, McCormick PC: Infections of the dural
spaces. Neurosurg Clin North Am 3:421-433, 1992.
13. Powers KS: Diagnosis and management of com-
mon toxic ingestions and inhalations. Pediatr Ann 29:
330-347, 2000.
14. Spirko BA, Wiley JF, III: Serotonin syndrome: A
new pediatric intoxication. Pediatr Emerg Care 15:440-
443, 1999.
15. Jacobs ES, Dickstein DP, Liebelt EL: Novel psych-
otropic medications in children: New toxicities to master.
Pediatr Emerg Care 17:226-231, 2001.
16. Towne AR, Waterhouse EF, Boggs JG, et al: Prev-
alence of nonconvulsive status epilepticus in comatose
patients. Neurology 54:1421-1423, 2000.
17. Birkhahn R, Fiorini M, Gaeta TJ: Painless intus-
susception and altered mental status. Am J Emerg Med
17:345-347, 1999.
18. Luks FI, Yazbeck S, Perreault G, et al: Changes in
the presentation of intussusception. Am J Emerg Med
10:574-576, 1992.
19. Grimm PC, Ogborn MR: Hemolytic uremic syn-
drome: The most common cause of acute renal failure in
childhood. Peditr Ann 23:505-511, 1994.
20. Ghajar J, Hariri RJ: Management of pediatric head
injury. Pediatr Clin North Am 39:1093-1125, 1992.
21. Conway EE: Nonaccidental head injury in infants:
The shaken baby syndrome revisited. Pediatr Ann 27:
677-690, 1998.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.