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munication that makes consciousness possible. Loss of consciousness can result from a
bilateral cerebral disturbance, an RAS disturbance, or both. Cerebral dysfunction characteristically produces the least dramatic decrease
in a patient’s LOC. In contrast, dysfunction of
the RAS produces the most dramatic decrease
in LOC—coma.
The most sensitive indicator of decreased
LOC is a change in the patient’s mental status.
The Glasgow Coma Scale, which measures a
patient’s ability to respond to verbal, sensory,
and motor stimulation, can be used to quickly
evaluate a patient’s LOC.
EMERGENCY INTERVENTIONS After
evaluating the patient’s airway, breathing,
and circulation, use the Glasgow Coma Scale to
quickly determine his LOC and to obtain baseline
data. (See Using the Glasgow Coma Scale, page
422.) If the patient’s score is 13 or less, emergency
surgery may be necessary. Insert an artificial airway, elevate the head of the bed 30 degrees and, if
spinal cord injury has been ruled out, turn the patient’s head to the side. Prepare to suction the patient if necessary. You may need to hyperventilate
him to reduce carbon dioxide levels and decrease
intracranial pressure (ICP). Then determine the
rate, rhythm, and depth of spontaneous respirations. Support his breathing with a handheld resuscitation bag, if necessary. If the patient’s Glasgow Coma Scale score is 7 or less, intubation and
resuscitation may be necessary.
Continue to monitor the patient’s vital signs,
being alert for signs of increasing ICP, such as
bradycardia and widening pulse pressure. When
his airway, breathing, and circulation are stabilized, perform a neurologic examination.
H
ISTORY AND PHYSICAL
EXAMINATION
Try to obtain history information from the patient, if he’s lucid, and from his family. Did the
patient complain of headache, dizziness, nausea, visual or hearing disturbances, weakness,
fatigue, or any other problems before his LOC
decreased? Has his family noticed any changes
in the patient’s behavior, personality, memory,
or temperament? Also ask about a history of
neurologic disease, cancer, or recent trauma or
infections; drug and alcohol use; and the development of other signs and symptoms.
Because decreased LOC can result from a
disorder affecting virtually any body system, tailor the remainder of your evaluation according
to the patient’s associated symptoms.
M
EDICAL CAUSES
◆ Adrenal crisis. Decreased LOC, ranging
from lethargy to coma, may develop within
8 to 12 hours of onset. Early associated findings
include progressive weakness, irritability,
anorexia, headache, nausea and vomiting, diarrhea, abdominal pain, and fever. Later signs and
symptoms include hypotension; rapid, thready
pulse; oliguria; cool, clammy skin; and flaccid
extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented
skin and mucous membranes.
◆ Brain abscess. Decreased LOC varies from
drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms—
constant intractable headache, nausea, vomiting, and seizures—reflect increasing ICP. Typical
later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality)
and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.
◆ Brain tumor. LOC decreases slowly, from
lethargy to coma. The patient may also experience apathy, behavior changes, memory loss,
decreased attention span, morning headache,
dizziness, vision loss, ataxia, and sensorimotor
disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance,
such as fluid retention or amenorrhea. Signs
and symptoms vary according to the location
and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and widening pulse
pressure also appear. In the final stages, the
patient may exhibit decorticate or decerebrate
posture.
◆ Cerebral aneurysm (ruptured). Somno-
lence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with
severe bleeding, which can be fatal. Onset is
usually abrupt, with sudden, severe headache,
nausea, and vomiting. Nuchal rigidity, back and
leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision point to
meningeal irritation. The type and severity of
other findings vary with the site and severity of
the hemorrhage and may include hemiparesis,
hemisensory defects, dysphagia, and visual
defects.
◆ Cerebral contusion. Usually unconscious
for a prolonged period, the patient may develop
dilated, nonreactive pupils and decorticate or
decerebrate posture. If he’s conscious or recovers consciousness, he may be drowsy, confused,
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Using the Glasgow Coma Scale
The Glasgow Coma Scale describes a patient’s baseline mental status and helps to detect and interpret changes from baseline findings. When using the Glasgow Coma Scale, test the patient’s
ability to respond to verbal, motor, and sensory stimulation, and grade your findings according
to the scale. A score of 15 indicates that the patient is alert, can follow simple commands, and is
oriented to time, place, and person. A decreased score in one or more categories may signal an
impending neurologic crisis. A score of 7 or less indicates severe neurologic damage.
Test
Eye-opening response
Spontaneously
To speech
To pain
None
Motor response
Obeys
Localizes
Withdraws
Abnormal flexion
Abnormal extension
Score
4
3
2
1
6
5
4
3
2
Response
Opens eyes spontaneously
Opens eyes when told to
Opens eyes only to painful stimulus
Doesn’t open eyes in response to stimuli
Shows two fingers when asked
Reaches toward painful stimulus and tries to remove it
Moves away from painful stimulus
Assumes a decorticate posture (shown below)
Assumes a decerebrate posture (shown below)
None
Verbal response (to question, “What year is this?”)
Oriented
Confused
Inappropriate words
Incomprehensible
No response
Total score
1
5
4
3
2
1
(3 to 15)
No response; just lies flaccid (an ominous sign)
Tells correct year
Tells incorrect year
Replies randomly with incorrect words
Moans or screams
No response
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disoriented, agitated, or even violent. Associated findings include blurred or double vision,
fever, headache, pallor, diaphoresis, tachycardia, altered respirations, aphasia, and hemiparesis. Residual effects include seizures, impaired mental status, slight hemiparesis, and
vertigo.
◆ Diabetic ketoacidosis. This disorder pro-
duces a rapid decrease in LOC, ranging from
lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient
may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; fruity breath odor;
Kussmaul’s respirations; warm, dry skin; and a
rapid, thready pulse. Untreated, this condition
invariably leads to coma and death.
◆ Encephalitis. Within 24 to 48 hours after on-
set, the patient may develop LOC changes ranging from lethargy to coma. Other possible findings include abrupt onset of fever, headache,
nuchal rigidity, nausea, vomiting, irritability,
personality changes, seizures, aphasia, ataxia,
hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.
◆ Encephalomyelitis (postvaccinal). This life-
threatening disorder produces rapid LOC deterioration from drowsiness to coma. The patient
also experiences rapid onset of fever, headache,
nuchal rigidity, back pain, vomiting, and
seizures.
◆ Encephalopathy. With hepatic encephalopa-
thy, signs and symptoms develop in four stages:
in the prodromal stage, slight personality
changes (disorientation, forgetfulness, slurred
speech) and slight tremor; in the impending
stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy,
aberrant behavior, and apraxia; in the stuporous
stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the
comatose stage, coma with decerebrate posture, hyperactive reflexes, positive Babinski’s
reflex, and fetor hepaticus.
With life-threatening hypertensive encephalopathy, LOC progressively decreases
from lethargy to stupor to coma. Besides
markedly elevated blood pressure, the patient
may experience severe headache, vomiting,
seizures, visual disturbances, transient paralysis, and eventually Cheyne-Stokes respirations.
With hypoglycemic encephalopathy, LOC
rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness,
restlessness, agitation, and confusion; hunger;
alternate flushing and cold sweats; and
headache, trembling, and palpitations. Blurred
vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, decreased pulse rate,
shallow respirations, and seizures. Flaccidity
and decerebrate posture appear late.
Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in LOC, leading to coma and brain death.
Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and
assessment reveals decreased pulse, blood
pressure, and deep tendon reflexes (DTRs);
Babinski’s reflex; absent doll’s eye sign; and
fixed pupils.
With uremic encephalopathy, LOC decreases
gradually from lethargy to coma. Early on, the
patient may appear apathetic, inattentive, confused, and irritable and may complain of
headache, nausea, fatigue, and anorexia. Other
findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias,
dyspnea, crackles, oliguria, and Kussmaul’s and
Cheyne-Stokes respirations.
◆ Epidural hemorrhage (acute). This life-
threatening posttraumatic disorder produces
momentary loss of consciousness, sometimes
followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting,
and bladder distention. Rapid deterioration in
consciousness follows, possibly leading to
coma. Other findings include irregular respirations, seizures, decreased and bounding pulse,
increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate
posture, and Babinski’s reflex.
◆ Heatstroke. As body temperature increases,
LOC gradually decreases from lethargy to
coma. Early signs and symptoms include
malaise, tachycardia, tachypnea, orthostatic
hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious,
and dizzy and may report a severe headache.
At the onset of heatstroke, the patient’s skin is
hot, flushed, and diaphoretic with blotchy
cyanosis; later, when his fever exceeds 105⬚ F
(40.5⬚ C), his skin becomes hot, flushed, and
anhidrotic. Pulse and respiratory rate increase
markedly, and blood pressure drops precipitously. Other findings include vomiting,
diarrhea, dilated pupils, and Cheyne-Stokes
respirations.
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◆ Hypercapnia with pulmonary syndrome.
LOC decreases gradually from lethargy to coma
(usually not prolonged). The patient becomes
confused or drowsy and develops asterixis and
muscle twitching. He may complain of headache
and exhibit mental dullness, papilledema, and
small, reactive pupils.
◆ Hypernatremia. This disorder, life-threaten-
ing if acute, causes LOC to deteriorate from
lethargy to coma. The patient is irritable and
exhibits twitches progressing to seizures. Other
associated signs and symptoms include a weak,
thready pulse; nausea; malaise; fever; thirst;
flushed skin; and dry mucous membranes.
◆ Hyperosmolar hyperglycemic nonketotic
syndrome. LOC decreases rapidly from lethargy
to coma. Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the
patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.
◆ Hyperventilation syndrome. Brief episodes
of unconsciousness follow stress-induced deep,
rapid breathing associated with anxiety and agitation. Associated findings include dizziness,
circumoral and peripheral paresthesia, twitching, carpopedal spasm, and arrhythmias.
◆ Hypokalemia. LOC gradually decreases to
lethargy; coma is rare. Other findings include
confusion, nausea, vomiting, diarrhea, and
polyuria; weakness, decreased reflexes, and
malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.
◆ Hyponatremia. This disorder, life-threaten-
ing if acute, produces decreased LOC in late
stages. Early nausea and malaise may progress
to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.
◆ Hypothermia. With severe hypothermia (tem-
perature below 90⬚ F [32.2⬚ C]), LOC decreases
from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by
cardiopulmonary arrest. With mild to moderate
hypothermia, the patient may experience memory
loss and slurred speech as well as shivering,
weakness, fatigue, and apathy. Other early signs
and symptoms include ataxia, muscle stiffness,
and hyperactive DTRs; diuresis; tachycardia and
decreased respiratory rate and blood pressure;
and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe
hypotension, decreased respiratory rate with
shallow respirations, and oliguria.
◆ Intracerebral hemorrhage. This life-
threatening disorder produces a rapid, steady
loss of consciousness within hours, commonly
accompanied by severe headache, dizziness,
nausea, and vomiting. Associated signs and
symptoms vary and may include increased
blood pressure, irregular respirations, Babinski’s
reflex, seizures, aphasia, decreased sensations,
hemiplegia, decorticate or decerebrate posture,
and dilated pupils.
◆ Listeriosis. If this serious infection spreads
to the nervous system and causes meningitis,
signs and symptoms include decreased LOC,
fever, headache, and nuchal rigidity. Early signs
and symptoms of listeriosis include fever, myalgias, abdominal pain, nausea, vomiting, and
diarrhea.
GENDER CUE Infections during pregnancy
may lead to premature delivery, infection of
the neonate, or stillbirth.
◆ Meningitis. Confusion and irritability are ex-
pected; however, stupor, coma, and seizures
may occur in those with severe meningitis.
Fever develops early, possibly accompanied by
chills. Associated findings include severe
headache, nuchal rigidity, hyperreflexia and,
possibly, opisthotonos. The patient exhibits
Kernig’s and Brudzinski’s signs and, possibly,
ocular palsies, photophobia, facial weakness,
and hearing loss.
◆ Myxedema crisis. The patient may exhibit a
swift decline in LOC. Other findings include severe hypothermia, hypoventilation, hypotension, bradycardia, hypoactive reflexes, periorbital and peripheral edema, impaired hearing
and balance, and seizures.
◆ Pontine hemorrhage. A sudden, rapid de-
crease in LOC to the point of coma occurs within minutes and death within hours. The patient
may also exhibit total paralysis, decerebrate
posture, Babinski’s reflex, absent doll’s eye sign,
and bilateral miosis (however, the pupils remain
reactive to light).
◆ Seizure disorders. A complex partial seizure
produces decreased LOC, manifested as a blank
stare, purposeless behavior (picking at clothing,
wandering, lip smacking or chewing motions),
and unintelligible speech. The seizure may be
heralded by an aura and followed by several
minutes of mental confusion.
An absence seizure usually involves a brief
change in LOC, indicated by blinking or eye
rolling, blank stare, and slight mouth movements.
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A generalized tonic-clonic seizure typically
begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored
breathing, apnea, and cyanosis may also occur.
Consciousness returns after the seizure, but the
patient remains confused and may have difficulty
talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness
and may fall into deep sleep.
An atonic seizure produces sudden unconsciousness for a few seconds.
Status epilepticus, rapidly recurring seizures
without intervening periods of physiologic recovery and return of consciousness, can be life
threatening.
◆ Shock. Decreased LOC—lethargy progressing
to stupor and coma—occurs late in shock. Associated findings include confusion, anxiety, and
restlessness; hypotension; tachycardia; weak
pulse with narrowing pulse pressure; dyspnea;
oliguria; and cool, clammy skin.
Hypovolemic shock is generally the result of
massive or insidious bleeding, either internally
or externally. Cardiogenic shock may produce
chest pain or arrhythmias and signs of heart
failure, such as dyspnea, cough, edema, jugular
vein distention, and weight gain. Septic shock
may be accompanied by high fever and chills.
Anaphylactic shock usually involves stridor.
◆ Stroke. LOC changes vary in degree and on-
set, depending on the lesion’s size and location
and the presence of edema. A thrombotic stroke
usually follows multiple transient ischemic attacks (TIAs). LOC changes may be abrupt or
take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach
their peak almost at once. Deficits associated
with a hemorrhagic stroke usually develop over
minutes or hours.
Associated findings vary with stroke type and
severity and may include disorientation; intellectual deficits, such as memory loss and poor
judgment; personality changes; and emotional
lability. Other possible findings include
dysarthria, dysphagia, ataxia, aphasia, apraxia,
agnosia, unilateral sensorimotor loss, and visual disturbances. In addition, urine retention, incontinence, constipation, headache, vomiting,
and seizures may occur.
◆ Subdural hematoma (chronic). LOC deteri-
orates slowly. Other signs and symptoms include confusion, decreased ability to concentrate, and personality changes accompanied by
headache, light-headedness, seizures, and a
dilated ipsilateral pupil with ptosis.
◆ Subdural hemorrhage (acute). With this
potentially life-threatening disorder, agitation
and confusion are followed by progressively decreasing LOC from somnolence to coma. The
patient may also experience headache, fever,
unilateral pupil dilation, decreased pulse and
respiratory rates, widening pulse pressure,
seizures, hemiparesis, and Babinski’s reflex.
◆ Thyroid storm. LOC decreases suddenly and
can progress to coma. Irritability, restlessness,
confusion, and psychotic behavior precede the
deterioration. Associated signs and symptoms
include tremors and weakness; visual disturbances; tachycardia, arrhythmias, angina, and
acute respiratory distress; warm, moist, flushed
skin; and vomiting, diarrhea, and fever to 105⬚ F
(40.5⬚ C).
◆ TIA. LOC decreases abruptly (with varying
severity) and gradually returns to normal within
24 hours. Site-specific findings may include vision loss, nystagmus, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus,
paresthesia, staggering or incoordinated gait,
aphasia, or dysphagia.
◆ West Nile encephalitis. This brain infection
is caused by the West Nile virus, a mosquitoborne flavivirus commonly found in Africa,
West Asia, and the Middle East and, less commonly, in the United States. Mild infection is
common. Signs and symptoms include fever,
headache, and body aches, commonly with
skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation,
coma, tremors, occasional seizures, paralysis
and, rarely, death.
O
THER CAUSES
◆ Alcohol. Alcohol use causes varying degrees
of sedation, irritability, and incoordination; intoxication commonly causes stupor.
◆ Drugs. Sedation and other degrees of de-
creased LOC can result from an overdose of a
barbiturate, another central nervous system depressant, or aspirin.
◆ Poisoning. Toxins, such as lead, carbon
monoxide, and snake venom, can cause varying
degrees of decreased LOC. Confusion is common, as are headache, nausea, and vomiting.
Other general features include hypotension,
cardiac arrhythmias, dyspnea, sensorimotor
loss, and seizures.
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S
PECIAL CONSIDERATIONS
Reassess the patient’s LOC and neurologic status
at least hourly. Carefully monitor ICP and intake
and output. Ensure airway patency and proper
nutrition. Take precautions to help ensure the
patient’s safety. Keep him on bed rest with the
side rails up and maintain seizure precautions.
Keep emergency resuscitation equipment at the
patient’s bedside. Prepare the patient for a computed tomography scan of the head, magnetic
resonance imaging of the brain, EEG, and lumbar puncture. Maintain an elevation of the head
of the bed to at least 30 degrees. Don’t administer an opioid or sedative because either may further decrease the patient’s LOC and hinder an
accurate, meaningful neurologic examination.
Apply restraints only if necessary because their
use may increase his agitation and confusion.
Talk to the patient even if he appears comatose;
your voice may help reorient him to reality.
P
EDIATRIC POINTERS
The primary cause of decreased LOC in children
is head trauma, which often results from physical abuse or a motor vehicle accident. Other
causes include accidental poisoning, hydrocephalus, and meningitis or brain abscess following an ear or respiratory infection. To reduce
the parents’ anxiety, include them in the child’s
care. Offer them support and realistic explanations of their child’s condition.
Lid lag
[Graefe’s sign]
A cardinal sign of thyrotoxicosis, lid lag is the
inability of the upper eyelid to follow the eye’s
downward movements. Testing for lid lag involves holding a finger, penlight, or other target
above the patient’s eye level and then moving it
downward and observing eyelid movement as
his eyes follow the target. This sign is demonstrated when a rim of sclera appears between
the upper lid margin and the iris when the patient lowers his eyes, when one lid closes more
slowly than the other, or when both lids close
slowly and incompletely with jerky movements.
H
ISTORY AND PHYSICAL
EXAMINATION
Because the patient isn’t generally able to recognize a lid lag himself, ask a friend or family
member if he has noticed it. If so, ask when he
first noticed lid lag or its possible manifestation,
incomplete closure of the eyelid. Explore other
signs and symptoms, and ask about a history of
thyroid disease. Next, perform a physical examination, focusing on the effects of thyrotoxicosis,
such as an enlarged thyroid, diaphoresis,
tremors, and exophthalmos.
M
EDICAL CAUSES
◆ Thyrotoxicosis. This disorder may produce
bilateral lid lag and other ocular effects, including exophthalmos, infrequent blinking, eye dryness and discomfort, conjunctival injection, and
a characteristic stare. (Thyrotoxicosis is the
most common cause of unilateral and bilateral
exophthalmos in adults and children.) Restricted
eye movement may produce diplopia. Other effects include an enlarged thyroid, nervousness,
heat intolerance, weight loss despite increased
appetite, diaphoresis, diarrhea, tremors, palpitations, widened pulse pressure, and silkensmooth skin texture.
Because thyrotoxicosis affects virtually every
body system, it can produce many other findings. For example, central nervous system effects include clumsiness, shaky handwriting,
and emotional lability. Integumentary effects include smooth, warm, flushed, and thickened
skin with itchy patches; fine, soft hair with premature graying and increased loss; friable nails;
and onycholysis.
Cardiopulmonary involvement causes constant dyspnea; tachycardia; full, bounding pulse;
widened pulse pressure; visible point of maximal
impulse; and, occasionally, systolic murmur.
Besides nausea and vomiting, GI findings include anorexia, diarrhea, and hepatomegaly.
Musculoskeletal findings include weakness,
fatigue, and atrophy, along with paralysis and,
occasionally, acropachy. Women may report
oligomenorrhea or amenorrhea; men may develop gynecomastia; both sexes may experience
decreased libido.
S
PECIAL CONSIDERATIONS
If lid lag is accompanied by exophthalmos, provide privacy to ease the patient’s self-consciousness. Don’t cover the affected eye with a gauze
pad or other object because removal could destroy the corneal epithelium. Help the patient
keep his eyes lubricated with saline drops.
P
EDIATRIC POINTERS
Children may have lid lag associated with aberrant regeneration of cranial nerve III or, rarely,
thyrotoxicosis.
P
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ATIENT COUNSELING
Stress the importance of complying with drug
therapy (such as antithyroid drugs or therapeutic radioactive iodine). Subtotal thyroidectomy
may be required in rare cases.
Light flashes
[Photopsias]
A cardinal symptom of vision-threatening retinal detachment, light flashes can occur locally
or throughout the visual field. The patient usually reports seeing spots, stars, or lightning-type
streaks. Flashes can occur suddenly or gradually
and can indicate temporary or permanent vision
impairment.
In most cases, light flashes signal the splitting
of the posterior vitreous membrane into two
layers; the inner layer detaches from the retina,
and the outer layer remains fixed to it. The sensation of light flashes may result from vitreous
traction on the retina, hemorrhage caused by a
tear in the retinal capillary, or strands of solid
vitreous floating in a local pool of liquid
vitreous.
EMERGENCY INTERVENTIONS Until reti-
nal detachment is ruled out, restrict the
patient’s eye and body movement.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient when the light flashes began.
Can he pinpoint their location, or do they occur
throughout the visual field? If the patient is experiencing eye pain or headache, have him describe it. Ask if the patient wears or has ever
worn corrective lenses and if he or a family
member has a history of eye or vision problems.
Also ask if the patient has other medical
problems—especially hypertension or diabetes
mellitus, which can cause retinopathy and, possibly, retinal detachment. Obtain an occupational history because light flashes may be related
to job stress or eye strain.
Next, perform a complete eye and vision examination, especially if trauma is apparent or
suspected. Begin by inspecting the external eye,
lids, lashes, and tear puncta for abnormalities
and the iris and sclera for signs of bleeding. Observe pupillary size and shape; check for reaction to light, accommodation, and consensual
light response. Then test visual acuity in each
eye. Also test visual fields; document any light
flashes that the patient reports during this test.
LOW BIRTH WEIGHT
M
EDICAL CAUSES
◆ Head trauma. A patient who has sustained
minor head trauma may report “seeing stars”
when the injury occurs. He may also complain
of localized pain at the injury site, generalized
headache, and dizziness. Later, he may develop
nausea, vomiting, and decreased level of consciousness.
◆ Migraine headache. Light flashes—possibly
accompanied by an aura—may herald a classic
migraine headache. As these symptoms subside, the patient typically experiences a severe,
throbbing, unilateral headache that usually lasts
1 to 12 hours and may be accompanied by
paresthesia of the lips, face, or hands; slight
confusion; dizziness; photophobia; nausea; and
vomiting.
◆ Retinal detachment. Light flashes described
as floaters or spots are localized in the portion
of the visual field where the retina is detaching.
With macular involvement, the patient may experience painless visual impairment resembling
a curtain covering the visual field.
◆ Vitreous detachment. Visual floaters may
accompany a sudden onset of light flashes. Usually, one eye is affected at a time.
S
PECIAL CONSIDERATIONS
If the patient has retinal detachment, prepare
him for reattachment surgery. Explain that after
surgery he may need to continue wearing bilateral eye patches and may have activity and
position restrictions until the retina heals
completely.
If the patient doesn’t have retinal detachment, reassure him that his light flashes are
temporary and don’t indicate eye damage. For
the patient with a migraine headache, maintain
a quiet, darkened environment; encourage
sleep; and administer an analgesic, as ordered.
P
EDIATRIC POINTERS
Children may experience light flashes after minor head trauma.
427
Low birth weight
Two groups of neonates are born weighing less
than the normal minimum birth weight of 5
(2,500 g)—those who are born prematurely (before the 37th week of gestation) and those who
are small for gestational age (SGA). The premature neonate weighs an appropriate amount for
his gestational age and probably would have
1
⁄2lb
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matured normally if carried to term. Conversely,
the SGA neonate weighs less than the normal
amount for his age; however, his organs are
mature. Differentiating between the two groups,
helps direct the search for a cause.
In the premature neonate, low birth weight
usually results from a disorder that prevents the
uterus from retaining the fetus, interferes with
the normal course of pregnancy, causes premature separation of the placenta, or stimulates
uterine contractions before term. In the SGA
neonate, intrauterine growth may be retarded
by a disorder that interferes with placental
circulation, fetal development, or maternal
health. (See Maternal causes of low birth weight.)
Regardless of the cause, low birth weight is
associated with higher neonate morbidity and
mortality; in fact, these neonates are 20 times
more likely to die within the first month of life.
Low birth weight can also signal a life-threatening emergency.
SGA neonates who will demonstrate catchup growth, do so by 8 to 12 months. Some SGA
neonates will remain below the 10th percentile.
Weights of the premature neonate should be
corrected for gestational age by approximately
24 months.
EMERGENCY INTERVENTIONS Because
low birth weight may be associated with
poorly developed body systems, particularly the
respiratory system, your priority is to monitor the
neonate’s respiratory status. Be alert for signs of
distress, such as apnea, grunting respirations, intercostal or xiphoid retractions, or a respiratory
rate exceeding 60 breaths/minute after the first
hour of life. If you detect any of these signs, prepare to provide respiratory support. Endotracheal
intubation or supplemental oxygen with an oxygen hood may be needed.
Monitor the neonate’s axillary temperature. Decreased fat reserves may keep him from maintaining normal body temperature, and a drop below
97.8⬚ F (36.5⬚ C) exacerbates respiratory distress
by increasing oxygen consumption. To maintain
normal body temperature, use an overbed warmer
or an Isolette. (If these are unavailable, use a
wrapped rubber bottle filled with warm water, but
be careful to avoid hyperthermia.) Cover neonate’s
head to prevent heat loss.
H
ISTORY AND PHYSICAL
EXAMINATION
As soon as possible, evaluate the neonate’s
neuromuscular and physical maturity to determine gestational age. (See Ballard Scale for
calculating gestational age, pages 430 and 431.)
Follow with a routine neonatal examination.
M
EDICAL CAUSES
This section lists some fetal and placental causes of low birth weight as well as the associated
signs and symptoms present in the neonate at
birth.
◆ Chromosomal aberrations. Abnormalities
in the number, size, or configuration of chromosomes can cause low birth weight and possibly
multiple congenital anomalies in a premature or
SGA neonate. For example, a neonate with trisomy 21 (Down syndrome) may be SGA and
have prominent epicanthal folds, a flat-bridged
nose, a protruding tongue, palmar simian
creases, muscular hypotonia, and an umbilical
hernia.
◆ Cytomegalovirus infection. Although low
birth weight in this disorder is usually associated with premature birth, some neonates may be
SGA. Assessment at birth may reveal these classic signs: petechiae and ecchymoses, jaundice,
and hepatosplenomegaly, which increases for
several days. The neonate may also have a high
fever, lymphadenopathy, tachypnea, and dyspnea, along with prolonged bleeding at puncture
sites.
◆ Placental dysfunction. Low birth weight
and a wasted appearance occur in an SGA
neonate. The neonate may be symmetrically
short or may appear relatively long for his low
weight. Additional findings reflect the underlying cause. For example, if maternal hyperparathyroidism caused placental dysfunction,
the neonate may exhibit muscle jerking and
twitching, carpopedal spasm, ankle clonus,
vomiting, tachycardia, and tachypnea.
◆ Rubella (congenital). Usually, the low-birth-
weight neonate with this disease is born at term
but is SGA. A characteristic “blueberry muffin”
rash accompanies cataracts, purpuric lesions,
hepatosplenomegaly, and a large anterior
fontanel. Abnormal heart sounds, if present,
vary with the type of associated congenital
heart defect.
◆ Toxoplasmosis (congenital). The low-birth-
weight neonate may be either premature or
SGA and may have hydrocephalus or microcephalus. Associated findings include fever,
seizures, lymphadenopathy, hepatosplenomegaly,
jaundice, and rash. Other defects, which may
occur months or years later, include strabismus,
blindness, epilepsy, and mental retardation.
◆ Varicella (congenital). Low birth weight is
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accompanied by cataracts and skin vesicles.
S
PECIAL CONSIDERATIONS
To make up for low fat and glycogen stores in the
low-birth-weight neonate, initiate feedings as
soon as possible and continue to feed every 2 to
3 hours. Provide gavage or I.V. feeding for sick or
very premature neonates. Check abdominal girth
daily or more frequently if indicated, and check
stools for blood because increasing girth and
bloody stools may indicate necrotizing enterocolitis. A sepsis workup may be necessary if signs of
infection are associated with low birth weight.
Check the neonate’s vital signs every 15 minutes for the first hour and at least once every
hour thereafter until his condition stabilizes. Be
alert for changes in temperature or behavior,
feeding problems, respiratory distress, or periods of apnea—possible indications of infection.
Also, monitor blood glucose levels and watch
for signs and symptoms of hypoglycemia, such
as irritability, jitteriness, tremors, seizures, irregular respirations, lethargy, and a highpitched or weak cry. If the neonate is receiving
supplemental oxygen, carefully monitor arterial
blood gas values and the oxygen concentration
of inspired air to prevent retinopathy.
Monitor the neonate’s urine output by weighing diapers before and after voiding. Check
urine color, measure specific gravity, and test
for the presence of glucose, blood, or protein.
Also, watch for changes in the neonate’s skin
color because increasing jaundice may indicate
hyperbilirubinemia.
Encourage the parents to participate in their
neonate’s care to strengthen bonding, and
allow ample time for their questions.
LYMPHADENOPATHY
429
Maternal causes of low
birth weight
If the neonate is small for gestational age,
consider these possible maternal causes:
◆ acquired immunodeficiency syndrome
◆ alcohol or opioid abuse
◆ chronic maternal illness
◆ cigarette smoking
◆ hypertension
◆ hypoxemia
◆ malnutrition
◆ toxemia.
If the neonate is born prematurely, con-
sider these common maternal causes:
◆ abruptio placentae
◆ amnionitis
◆ cocaine or crack use
◆ incompetent cervix
◆ placenta previa
◆ polyhydramnios
◆ preeclampsia
◆ premature rupture of membranes
◆ severe maternal illness
◆ urinary tract infection.
page 432. See also Causes of localized lymphadenopathy, page 433.)
Normally, lymph nodes are discrete, mobile,
soft, nontender and, except in children, nonpalpable. (However, palpable nodes may be normal
in adults.) Nodes that are more than
in diameter are cause for concern. They may be
tender and the skin overlying the lymph node
may be erythematous, suggesting a draining lesion. Alternatively, they may be hard and fixed,
tender or nontender, suggesting a malignant
tumor.
3
⁄8” (1 cm)
Lymphadenopathy
Lymphadenopathy—enlargement of one or
more lymph nodes—may result from increased
production of lymphocytes or reticuloendothelial cells, or from infiltration of cells that aren’t
normally present. This sign may be generalized
(involving three or more node groups) or localized. Generalized lymphadenopathy may be
caused by an inflammatory process, such as
bacterial or viral infection, connective tissue
disease, an endocrine disorder, or neoplasm.
Localized lymphadenopathy most commonly results from infection or trauma affecting a specific area. (See Areas of localized lymphadenopathy,
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient when he first noticed the
swelling, and whether it’s located on one side of
his body or both. Are the swollen areas sore,
hard, or red? Ask the patient if he has recently
had an infection or other health problem. Also
ask if a biopsy has ever been done on any node
because this may indicate a previously diagnosed cancer. Find out if the patient has a family history of cancer.
Palpate the entire lymph node system to determine the extent of lymphadenopathy and to
detect any other areas of local enlargement. Use
the pads of your index and middle fingers to
430 LYMPHADENOPATHY
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Ballard Scale for calculating gestational age
Neuromuscular maturity
NEUROMUSCULAR MATURITY
MATURITY
SIGN
POSTURE
__
0345
SCORENEUROMUSCULAR
12-1
RECORD
SCORE
HERE
SQUARE
WINDOW
(Wrist)
ARM RECOIL
POPLITEAL
ANGLE
SCARF SIGN
HEEL TO EAR
Physical maturity
PHYSICAL MATURITY
MATURITY
SIGN
SKIN
LANUGO
PLANTAR
SURFACE
BREAST
>90° 90° 60° 45° 30° 0°
_
180° 160° 140° 120° 100° 90° <90°
Sticky,
friable,
transparent
None
Heel-toe
40 to
50 mm: –1;
<40 mm: –2
Imperceptible
<90°90° to 110°110° to 140°140° to 180°180°
TOTAL NEUROMUSCULAR
MATURITY SCORE
SCOREPHYSICAL
Gelatinous,
red, translucent
Sparse Abundant Thinning Bald areas Mostly bald
>50 mm;
no crease
Barely
perceptible
12-1 0 3 4 5
Smooth,
pink; visible
vessels
Faint red
marks
Flat areola,
no bud
Superficial
peeling or
rash; few visible vessels
Anterior
transverse
crease only
Stippled
areola; 1- to
2-mm bud
Cracking;
pale areas;
rare visible
vessels
Creases over
anterior twothirds
Raised
areola; 3- to
4-mm bud
Parchmentlike; deep
cracking; no
visible vessels
Creases over
entire sole
Full areola;
5- to 10-mm
bud
Leathery,
cracked,
wrinkled
_
_
_
_
RECORD
SCORE
HERE
_
_
_
Lids fused,
EYE AND EAR
GENITALIA,
(Male)
GENITALIA,
(Female)
Adapted with permission from Ballard, J. L. “New Ballard Scale Expanded To Include Extremely Premature Infants,”
Journal of Pediatrics 119:417-23, 1991.
loosely: –1;
tightly: –2
Scrotum flat,
smooth
Clitoris
prominent;
labia flat
Lids open;
pinna flat,
stays folded
Scrotum
empty; faint
rugae
Prominent
clitoris; small
labia minora
Slightly
curved pinna;
soft, slow
recoil
Testes in
upper canal;
rare rugae
Prominent
clitoris;
enlarging
minora
Well-curved
pinna; soft
but ready
recoil
Testes
descending;
few rugae
Majora and
minora
equally
prominent
Formed and
firm; instant
recoil
Testes down;
good rugae
Majora large;
minora small
Thick cartilage; ear stiff
Testes
pendulous;
deep rugae
Majora cover
clitoris and
minora
MATURITY SCORE
_
_
_
TOTAL PHYSICAL
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