Pediatric emergency medicine trisk 113

The neurologic examination of the comatose patient should include standard tests
of eye opening, responsiveness to verbal and tactile stimuli, and deep tendon
reflexes as well as the more specialized examinations described in this section.
Any focal (unilateral) abnormal finding is always significant because it may
indicate a structural CNS lesion. Abnormal findings on neurologic examination
reflect the underlying pathologic condition causing coma and may allow
localization of a lesion within the brain.
Patients with ALOC benefit from quantification of their impairment using
standard measurements, allowing evaluation and documentation of patients’
changing neurologic status over time. The effect of medical interventions may
then be more easily assessed. The use of accepted scoring systems also facilitates
communication with consultants such as neurologists and neurosurgeons. In
addition, many outcome measures of neurologically injured patients rely on
scales used to assess neurologic function. The most widely used measurement of
consciousness is the Glasgow Coma Scale (GCS) shown in Table 17.1 . Patients
are graded on three areas of neurologic function: Eye opening, motor response,
and verbal responsiveness. A GCS score of 3 is the minimum score possible and
represents complete unresponsiveness; a GCS score of 15 indicates a fully alert
patient.
Pupillary responses provide the most direct window to the brain of a comatose
patient. A unilaterally enlarging pupil (greater than 5 mm) that becomes
progressively less reactive to light indicates either progressive displacement of
the midbrain or medial temporal lobe, or downward displacement of the upper
brainstem. Bilateral enlarged and unreactive (“blown”) pupils indicate profound
CNS dysfunction and are most commonly seen with posttraumatic increases in
ICP. Nontraumatic conditions affecting the brain diffusely usually spare pupillary
responses. Exceptions include maximal constriction of pinpoint pupils caused by
opiate intoxication and minimal constriction of widely dilated pupils caused by
intoxication with anticholinergic agents.
Other ocular signs noted in patients with depressed consciousness are the
roving side-to-side conjugate eye movements seen in lighter stages of metabolic

coma. Persistent conjugate deviation of the eyes to one side may be caused by
focal seizure activity, its resultant postictal state, or focal lesions within the brain.
Ongoing seizure activity is usually apparent because of the jerking ocular
movements present but nonconvulsive status may present with coma only. Most
structural brainstem lesions abolish conjugate eye movements, but it is rare for a
metabolic disorder to do so. Deepening ALOC may also be measured by the
reduction and loss of spontaneous blinking, then loss of blinking caused by


touching the eyelashes, and finally loss of blink with corneal touch. Both eyes
should be tested to detect asymmetry.
Limb movement and postural changes seen in comatose patients include the
bilateral restless movements of the limbs of patients in light coma. Unilateral
jerking muscular movements may indicate focal seizure activity or generalized
convulsions in a patient with hemiparesis. Decerebrate rigidity refers to stiff
extension of limbs with internal rotation of the arms and plantar flexion of the
feet. It is not a posture that is held constantly; it usually occurs intermittently in
patients with midbrain compression, cerebellar lesions, or metabolic disorders.
Decorticate rigidity, when arms are held in flexion and adduction and legs are
extended, indicates CNS dysfunction at a higher anatomic level, usually in
cerebral white matter or internal capsule and thalamus. Signs of meningeal
irritation include Kernig sign, resistance to bent knee extension with the hip in 90
degrees flexion, and Brudzinski sign, involuntary knee and hip flexion with
passive neck flexion. In infants, meningeal irritation may be manifest as
paradoxic irritability, in which picking up the baby to soothe results in pain and
worsening crying.
The abnormal breathing pattern most commonly seen in comatose patients is
Cheyne–Stokes respirations, where intervals of waxing and waning hyperpnea
alternate with short periods of apnea. Other abnormal breathing patterns that
occur with brainstem lesions include central neurogenic hyperventilation, which

can produce respiratory alkalosis, and apneustic breathing, in which a 2- to 3second pause occurs during each full inspiration.

Laboratory and Radiologic Studies
Immediate bedside glucose, sodium, blood gas, and hemoglobin determination
should be performed on every patient with nontraumatic ALOC. Other laboratory
tests indicated for evaluation of coma in the absence of trauma include
electrolytes, blood urea nitrogen, creatinine, blood gas, hemoglobin, hematocrit,
osmolality, ammonia, and antiepileptic levels. Toxicologic screening of both
blood and urine should be obtained in patients with ALOC of unknown origin. A
noncontrast CT scan of the brain can reveal many causes of coma, such as
cerebral edema, hydrocephalus, malignancy, hematomas, and abscesses.
Infarction, thrombosis, and inflammatory conditions may require the addition of
contrast or the use of magnetic resonance imaging.

Vital Sign Abnormalities
Evaluation and treatment of airway, breathing, and circulatory compromise
always take precedence in the child with ALOC. Both airway patency and


respiratory effort may be compromised by decreased mental status and may result
in hypoxia and/or hypercarbia. The former may be readily measured using pulse
oximetry, although values will be inaccurate if a toxic hemoglobinopathy, such as
methemoglobinemia or carboxyhemoglobinemia, is present. The adequacy of
ventilation can be assessed clinically with a stethoscope and can be quantified by
continuously monitoring end-tidal CO2 (see Chapter 21 Cyanosis ). Arterial blood
gas analysis with co-oximetry is useful to quantify respiratory and acid–base
status and to identify altered hemoglobin states.
The numerical definition of hypotension varies with age, but pallor and
evidence of poor peripheral perfusion, with prolonged capillary refill time, is
recognizable even before placement of a sphygmomanometer cuff. Immediate

administration of IV crystalloid therapy starting with 20 mL/kg of normal saline
or lactated Ringer solution is indicated, followed by additional boluses and
vasopressors if needed. Of the empiric antidotal therapies often used in adults,
only glucose (0.25 to 0.5 g/kg) is routinely administered to children. An empiric
trial of naloxone (0.1 mg/kg, max 2 mg/dose) is sometimes justified, whereas
flumazenil and thiamine are given only for specific indications (see Chapter 102
Toxicologic Emergencies ).
Severe hypertension is less easily discerned on physical examination. If
confirmed in more than one extremity, antihypertensives should be administered
via the IV route (see Chapters 37 Hypertension and 100 Renal and Electrolyte
Emergencies ). Mental status should improve after blood pressure is lowered to
high normal levels. Patients in hypertensive crises are at risk for hemorrhagic
stroke and should be evaluated with a head CT scan if they are neurologically
abnormal after blood pressure lowering. Hypertension in the comatose patient
after traumatic injury may represent a physiologic response to increased ICP to
allow maintenance of cerebral perfusion pressure by raising mean arterial
pressure. In this context, elevated blood pressure should not be lowered with
antihypertensives; treatment instead should be aimed at decreasing ICP.
Hypothermia and hyperthermia are readily recognized once a core (rectal)
temperature less than 35°C or greater than 41°C is obtained. The mental status of
these patients should begin to improve as body temperature approaches the
normal range. A significant percentage of patients with abnormal core
temperatures have drowned, fallen through ice, or were engaged in sporting
activities in extreme environments or without adequate hydration. Adolescents
with hypothermia may have associated ethanol toxicity. Head trauma, hypoxia,
and/or cervical spine injury may be present in these patients.


History of Head Trauma
The patient with deeply depressed consciousness (GCS score less than 9) after

head trauma is presumed to have increased ICP until proven otherwise. Rapid
sequence intubation is indicated to protect the airway and to maintain effective
ventilation. Cervical spine injury should be assumed and cervical immobilization
maintained at all times. An emergent noncontrast brain CT scan should be
obtained and neurosurgery consulted. Elevation of the head of the bed to 30
degrees and maintenance of the midline position of the head are simple
nonpharmacologic maneuvers to try to reduce ICP. In cases when immediate but
necessary neurosurgical intervention is not possible for intracranial hemorrhage
(e.g., extended transport time) or in cases of diffuse cerebral edema, 3% saline or
mannitol may be helpful to treat elevated ICP.

History of Seizures
The patient with ALOC in the absence of trauma should be evaluated for recent
seizure activity with current postictal state (see Chapters 72 Seizures and 97
Neurologic Emergencies ). A history of previous seizures, witnessed convulsive
activity, and ALOC consistent with previous postictal periods are valuable clues
to this etiology of coma. Ongoing seizure activity may be revealed by the
presence of muscular twitching, increased tonicity, nystagmus, or eyelid
fluttering. Patients with subtle or completely nonconvulsive forms of status
epilepticus may exhibit tachycardia but may require an EEG to diagnose. The
mental status examination of the postictal patient should gradually improve over
several hours. Although temporary focal neurologic deficits (e.g., Todd paralysis)
may follow seizures, they must be presumed to indicate the presence of focal
CNS lesions until proven otherwise.
The evaluation of neurologically depressed patients with seizures varies based
on the patient’s history, type of seizure, and presence or absence of fever. Patients
with a history of seizures should have serum antiepileptic concentrations
measured and be observed until they approach their neurologic baseline. Children
who have had a simple febrile seizure (see Chapter 72 Seizures ) should return to
their baseline state soon, usually within 1 hour. Those who remain lethargic or

irritable past this point (especially after antipyretic administration) should be
suspected of having meningitis and are candidates for lumbar puncture.
Patients with new-onset generalized seizures who are afebrile warrant
additional evaluation. Depending on recent history (e.g., vomiting or diarrhea), it
may be advisable to check serum electrolytes or a toxicologic screen. Depending
on local resources and practice, patients with newly diagnosed afebrile seizures