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198 DECEREBRATE POSTURE
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Comparing decerebrate and decorticate postures
Decerebrate posture results from damage to the upper brain stem. In this posture, the arms are
adducted and extended, with the wrists pronated and the fingers flexed. The legs are stiffly extended, with plantar flexion of the feet.
Decorticate posture results from damage to one or both corticospinal tracts. In this posture, the
arms are adducted and the elbows are flexed, with the wrists and fingers flexed on the chest. The
legs are stiffly extended and internally rotated, with plantar flexion of the feet.
M
EDICAL CAUSES
◆ Brain stem infarction. Decerebrate posture
may be elicited when this primary lesion produces a coma. Associated signs and symptoms
vary with the severity of the infarct and may include cranial nerve palsies, bilateral cerebellar
ataxia, and sensory loss. In a deep coma, all
normal reflexes are usually lost, resulting in absence of doll’s eye sign, a positive Babinski’s
reflex, and flaccidity.
◆ Brain stem tumor. In a brain stem tumor,
decerebrate posture is a late sign that accompanies a coma. Early findings commonly include
hemiparesis or quadriparesis, cranial nerve
palsies, vertigo, dizziness, ataxia, and vomiting.
◆ Cerebral lesion. Whether the cause is trau-
ma, tumor, abscess, or infarction, any cerebral
lesion that increases ICP may also produce decerebrate posture, which is typically a late sign.
Associated findings vary with the lesion’s site
and extent but commonly include a coma, abnormal pupil size and response to light, and the
classic triad of increased ICP—bradycardia, increasing systolic blood pressure, and widening
pulse pressure.
◆ Hepatic encephalopathy. A late sign in this
disorder, decerebrate posture occurs with a
coma resulting from increased ICP and ammonia toxicity. Associated signs include fetor hepaticus (foul-smelling breath), a positive Babinski’s reflex, and hyperactive DTRs.
◆ Hypoglycemic encephalopathy. Character-
ized by extremely low blood glucose levels, this
disorder may produce decerebrate posture and
a coma. It also causes dilated pupils, bradypnea,
and bradycardia. Muscle spasms, twitching, and
seizures eventually progress to flaccidity.
◆ Hypoxic encephalopathy. Severe hypoxia
may produce decerebrate posture—the result of
brain stem compression associated with anaerobic metabolism and increased ICP. Other findings include a coma, a positive Babinski’s reflex,
absence of doll’s eye sign, hypoactive DTRs, and
possibly fixed pupils and respiratory arrest.
◆ Pontine hemorrhage. Typically, this life-
threatening disorder rapidly leads to decerebrate posture with a coma. Accompanying signs
include total paralysis, absence of doll’s eye
sign, a positive Babinski’s reflex, and small, reactive pupils.
DECORTICATE POSTURE 199
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◆ Posterior fossa hemorrhage. This subten-
torial lesion causes decerebrate posture. Its early signs and symptoms include vomiting,
headache, vertigo, ataxia, stiff neck, drowsiness, papilledema, and cranial nerve palsies.
The patient eventually slips into a coma and
may experience respiratory arrest.
O
THER CAUSES
◆ Diagnostic tests. Removal of spinal fluid
during a lumbar puncture to relieve high ICP
may precipitate cerebral compression of the
brain stem and cause decerebrate posture and a
coma.
S
PECIAL CONSIDERATIONS
Help prepare the patient for diagnostic tests
that will determine the cause of his decerebrate posture. These include skull X-rays, computed tomography scan, magnetic resonance
imaging, cerebral angiography, digital subtraction angiography, EEG, brain scan, and ICP
monitoring.
Monitor the patient’s neurologic status and
vital signs every 30 minutes or as indicated.
Also, be alert for signs of increased ICP (bradycardia, increasing systolic blood pressure, and
widening pulse pressure) and neurologic deterioration (altered respiratory pattern and abnormal temperature).
Inform the patient’s family that decerebrate
posture is a reflex response—not a voluntary response to pain or a sign of recovery. Offer emotional support.
P
EDIATRIC POINTERS
Children younger than age 2 may not display
decerebrate posture because the nervous system is still immature. However, if this posture
occurs, it’s usually the more severe
opisthotonos. In fact, opisthotonos is more
common in infants and young children than in
adults and is usually a terminal sign. In children, the most common cause of decerebrate
posture is head injury. It also occurs in Reye’s
syndrome—the result of increased ICP causing
brain stem compression.
Decorticate posture
[Decorticate rigidity, abnormal
flexor response]
A sign of corticospinal damage, decorticate posture is characterized by adduction of the arms
and flexion of the elbows, with wrists and fingers flexed on the chest. The legs are extended
and internally rotated, with plantar flexion of
the feet. This posture may occur unilaterally or
bilaterally. It usually results from a stroke or
head injury. It may be elicited by noxious stimuli
or may occur spontaneously. The intensity of
the required stimulus, the duration of the posture, and the frequency of spontaneous
episodes vary with the severity and location of
the cerebral injury.
Although a serious sign, decorticate posture
carries a more favorable prognosis than decerebrate posture. However, decorticate posture
may progress to decerebrate posture if the
causative disorder extends lower in the brain
stem. (See Comparing decerebrate and decorti-
cate postures.)
EMERGENCY INTERVENTIONS Obtain
vital signs and evaluate the patient’s level of
consciousness (LOC). If his consciousness is impaired, insert an oropharyngeal airway, and take
measures to prevent aspiration (unless spinal cord
injury is suspected). Evaluate the patient’s respiratory rate, rhythm, and depth. Prepare to assist respirations with a handheld resuscitation bag or
with intubation and mechanical ventilation if necessary. Also, institute seizure precautions.
H
ISTORY AND PHYSICAL
EXAMINATION
Test the patient’s motor and sensory function.
Evaluate pupil size, equality, and response to
light. Then test cranial nerve function and deep
tendon reflexes. Ask family members if the patient experienced headache, dizziness, nausea,
changes in vision, numbness, or tingling. When
did the patient first notice these symptoms?
Is his family aware of any behavioral changes?
Also, ask about a history of cerebrovascular disease, cancer, meningitis, encephalitis, upper
respiratory tract infection, bleeding or clotting
disorders, or recent trauma.
M
EDICAL CAUSES
◆ Brain abscess. Decorticate posture may oc-
cur in a brain abscess. Accompanying findings
vary depending on the size and location of the
abscess but may include aphasia, hemiparesis,
headache, dizziness, seizures, nausea, and
vomiting. The patient may also experience behavioral changes, altered vital signs, and decreased LOC.
◆ Brain tumor. A brain tumor may produce
decorticate posture that’s usually bilateral—the
200 DEEP TENDON REFLEXES, HYPERACTIVE
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result of increased intracranial pressure (ICP)
associated with tumor growth. Related signs
and symptoms include headache, behavioral
changes, memory loss, diplopia, blurred vision
or vision loss, seizures, ataxia, dizziness, apraxia, aphasia, paresis, sensory loss, paresthesia,
vomiting, papilledema, and signs of hormonal
imbalance.
◆ Head injury. Decorticate posture may result
from a head injury, depending on the site and
severity of the injury. Associated signs and
symptoms include headache, nausea and vomiting, dizziness, irritability, decreased LOC, aphasia, hemiparesis, unilateral numbness, seizures,
and pupillary dilation.
◆ Stroke. Typically, a stroke involving the cere-
bral cortex produces unilateral decorticate posture, also called spastic hemiplegia. Other signs
and symptoms include hemiplegia (contralateral
to the lesion), dysarthria, dysphagia, unilateral
sensory loss, apraxia, agnosia, aphasia, memory loss, decreased LOC, urine retention, urinary
incontinence, and constipation. Ocular effects
include homonymous hemianopsia, diplopia,
and blurred vision.
S
PECIAL CONSIDERATIONS
Monitor the patient’s neurologic status and vital
signs every 30 minutes to 2 hours. Be alert for
signs of increased ICP, including bradycardia,
increasing systolic blood pressure, and widening
pulse pressure and subtle signs of neurologic
deterioration.
P
EDIATRIC POINTERS
Decorticate posture is an unreliable sign before
age 2 because of nervous system immaturity. In
children, this posture usually results from head
injury, but it may also occur in Reye’s syndrome.
lesion above the level of the reflex arc being
tested may result in hyperactive DTRs. Abnormal
neuromuscular transmission at the end of the
reflex arc may also cause hyperactive DTRs. For
example, a deficiency of calcium or magnesium
may cause hyperactive DTRs because these electrolytes regulate neuromuscular excitability. (See
The reflex arc, pages 202 and 203.)
Although hyperactive DTRs typically accompany other neurologic findings, they usually lack
specific diagnostic value.
H
ISTORY AND PHYSICAL
EXAMINATION
After eliciting hyperactive DTRs, take the patient’s history. Ask about spinal cord injury or
other trauma and about prolonged exposure to
cold, wind, or water. Could the patient be pregnant? A positive response to any of these questions requires prompt evaluation to rule out
life-threatening autonomic hyperreflexia,
tetanus, preeclampsia, or hypothermia. Ask
about the onset and progression of associated
signs and symptoms. Next, perform a neurologic examination. Evaluate level of consciousness, and test motor and sensory function in
the limbs. Ask about paresthesia. Check for
ataxia or tremors and for speech and visual
deficits. Test for Chvostek’s sign (an abnormal
spasm of the facial muscles elicited by light
taps on the facial nerve in patients who have
hypocalcemia) and Trousseau’s sign (a carpal
spasm induced by inflating a sphygmomanometer cuff on the upper arm to a pressure
exceeding systolic blood pressure for 3 minutes
in patients who have hypocalcemia or hypomagnesemia) and for carpopedal spasm. Ask
about vomiting or altered urination habits. Be
sure to take vital signs.
Deep tendon reflexes,
hyperactive
A hyperactive deep tendon reflex (DTR) is an
abnormally brisk muscle contraction that occurs in response to a sudden stretch induced
by sharply tapping the muscle’s tendon of insertion. This elicited sign may be graded as
brisk or pathologically hyperactive. Hyperactive DTRs are commonly accompanied by
clonus.
The corticospinal tract and other descending
tracts govern the reflex arc—the relay cycle that
produces any reflex response. A corticospinal
M
EDICAL CAUSES
◆ Amyotrophic lateral sclerosis. This disor-
der produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the
patient develops atrophy of the neck and tongue
muscles, fasciculations, weakness of the legs
and, possibly, bulbar signs (dysphagia, dysphonia, facial weakness, and dyspnea).
◆ Brain tumor. A cerebral tumor causes
hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop
slowly and may include unilateral paresis or
paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
DEEP TENDON REFLEXES, HYPOACTIVE 201
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◆ Hepatic encephalopathy. Generalized hy-
peractive DTRs occur late and are accompanied
by a positive Babinski’s reflex, fetor hepaticus,
and a coma.
◆ Hypocalcemia. This disorder may produce
sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching
and cramping, positive Chvostek’s and
Trousseau’s signs, carpopedal spasm, and
tetany.
◆ Hypomagnesemia. This disorder results in
gradual onset of generalized hyperactive DTRs
accompanied by muscle cramps, hypotension,
tachycardia, paresthesia, ataxia, tetany and,
possibly, seizures.
◆ Hypothermia. Mild hypothermia (90 to 94 F
[32.2 to 34.4 C]) produces generalized hyperactive DTRs. Other signs and symptoms include
shivering, fatigue, weakness, lethargy, slurred
speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale
skin.
◆ Multiple sclerosis. Typically, hyperactive
DTRs are preceded by weakness and paresthesia in one or both arms or legs. Associated signs
include clonus and a positive Babinski’s reflex.
Passive flexion of the patient’s neck may cause
a tingling sensation down his back. Later, ataxia, diplopia, vertigo, vomiting, urine retention,
or urinary incontinence may occur.
◆ Preeclampsia. Occurring in pregnancy of at
least 20 weeks’ duration, preeclampsia may
cause gradual onset of generalized hyperactive
DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight
gain; edema of the face, fingers, and abdomen
after bed rest; albuminuria; oliguria; severe
headache; blurred or double vision; epigastric
pain; nausea and vomiting; irritability; cyanosis;
dyspnea; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
◆ Spinal cord lesion. Incomplete spinal cord
lesions cause hyperactive DTRs below the level
of the lesion. In a traumatic lesion, hyperactive
DTRs follow resolution of spinal shock. In a
neoplastic lesion, hyperactive DTRs gradually
replace normal DTRs. Other signs and symptoms are paralysis and sensory loss below the
level of the lesion, urine retention and overflow
incontinence, and alternating constipation and
diarrhea. A lesion above T6 may also produce
autonomic hyperreflexia with diaphoresis and
flushing above the level of the lesion, headache,
nasal congestion, nausea, increased blood pressure, and bradycardia.
◆ Stroke. Any stroke that affects the origin of
the corticospinal tracts causes sudden onset of
hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits,
spasticity, and a positive Babinski’s reflex.
◆ Tetanus. In this disorder, sudden onset of
generalized hyperactive DTRs accompanies
tachycardia, diaphoresis, low-grade fever,
painful and involuntary muscle contractions,
trismus (lockjaw), and risus sardonicus (a masklike grin).
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests to evaluate hyperactive DTRs. These may include laboratory tests for serum calcium magnesium and
ammonia levels, magnetic resonance imaging,
computed tomography scan, lumbar puncture,
spinal X-rays, and myelography.
If motor weakness accompanies hyperactive
DTRs, perform or encourage range-of-motion
exercises to preserve muscle integrity and prevent deep vein thrombosis. Also, reposition the
patient frequently, provide a special mattress,
and massage his back and ensure adequate nutrition to prevent skin breakdown. Administer a
muscle relaxant and a sedative to relieve severe
muscle contractions. Keep emergency resuscitation equipment on hand. Provide a quiet, calm
atmosphere to decrease neuromuscular excitability. Assist with activities of daily living,
and provide emotional support.
P
EDIATRIC POINTERS
Hyperreflexia may be a normal sign in neonates.
After age 6, reflex responses are similar to those
of adults. When testing DTRs in small children,
use distraction techniques to promote reliable
results.
Cerebral palsy commonly causes hyperactive
DTRs in children. Reye’s syndrome causes generalized hyperactive DTRs in stage II and absent
DTRs in stage V. Adult causes of hyperactive
DTRs may also appear in children.
Deep tendon reflexes,
hypoactive
A hypoactive deep tendon reflex (DTR) is an
abnormally diminished muscle contraction that
occurs in response to a sudden stretch induced
by sharply tapping the muscle’s tendon of
(Text continues on page 204.)
202 DEEP TENDON REFLEXES, HYPOACTIVE
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The reflex arc
The reflex arc is the transmission of sensory impulses to a motor neuron via the dorsal
root. The motor neuron delivers the impulse to a muscle or gland, producing an immediate
response.
Cerebral
cortex
SENSATION
Sensory
neuron
REFLEX ARC
Interneuron
Dorsal root
ganglion
REACTION
Motor
neuron
DEEP TENDON REFLEXES, HYPOACTIVE 203
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BICEPS REFLEX
(C 5–6 INNERVATION)
PATELLAR REFLEXES
(L 2–4 INNERVATION)
TRICEPS REFLEX
(C 7–8 INNERVATION)
BRACHIORADIALIS REFLEX
(C 5–6 INNERVATION)
ACHILLES TENDON REFLEX
(S 1–2 INNERVATION)
204 DEEP TENDON REFLEXES, HYPOACTIVE
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Documenting deep tendon reflexes
Record the patient’s deep tendon reflex
scores by drawing a stick figure and entering the grades on this scale at the
proper location. The figure shown here
indicates hypoactive deep tendon reflexes in the legs; other reflexes are normal.
KEY:
0 = absent
+ = hypoactive
(diminished)
++ = normal
+++ = brisk (increased)
++++ = hyperactive (clonus
may be present)
insertion. It may be graded as minimal (+) or
absent (0). Symmetrically reduced (+) reflexes
may be normal.
Normally, a DTR depends on an intact receptor, intact sensory-motor nerve fiber, an intact
neuromuscular-glandular junction, and a functional synapse in the spinal cord. Hypoactive
DTRs may result from damage to the reflex arc
involving the specific muscle, the peripheral
nerve, the nerve roots, or the spinal cord at that
level. Hypoactive DTRs are an important sign of
many disorders, especially when they appear
with other neurologic signs and symptoms. (See
Documenting deep tendon reflexes.)
H
ISTORY AND PHYSICAL
EXAMINATION
After eliciting hypoactive DTRs, obtain a thorough history from the patient or a family member. Have him describe current signs and symptoms in detail. Then take a family and drug
history.
Next, evaluate the patient’s level of consciousness. Test motor function in his limbs,
and palpate for muscle atrophy or increased
mass. Test sensory function, including pain,
touch, temperature, and vibration sensation.
Ask about paresthesia. To observe gait and coordination, have the patient take several steps.
To check for Romberg’s sign, ask him to stand
with his feet together and his eyes closed. During conversation, evaluate his speech. Check for
Brachioradialis
reflex
Biceps reflex
Triceps reflex
Patellar reflex
(knee)
Achilles tendon
reflex (ankle)
signs of vision or hearing loss. Abrupt onset of
hypoactive DTRs accompanied by muscle weakness may occur in life-threatening GuillainBarré syndrome, botulism, or spinal cord lesions
with spinal shock.
Look for autonomic nervous system effects
by taking vital signs and monitoring for increased heart rate and blood pressure. Also, inspect the skin for pallor, dryness, flushing, or
diaphoresis. Auscultate for hypoactive bowel
sounds, and palpate for bladder distention. Ask
about nausea, vomiting, constipation, and
incontinence.
M
EDICAL CAUSES
◆ Botulism. In this disorder, generalized hy-
poactive DTRs accompany progressive descending muscle weakness. Initially, the patient usually complains of blurred and double vision and,
occasionally, anorexia, nausea, and vomiting.
Other early bulbar findings include vertigo,
hearing loss, dysarthria, and dysphagia. The patient may have signs of respiratory distress and
severe constipation marked by hypoactive
bowel sounds.
◆ Cerebellar dysfunction. This disorder may
produce hypoactive DTRs by increasing the level of inhibition through long tracts upon spinal
motor neurons. Associated clinical findings vary
depending on the cause and location of the dysfunction.
DEEP TENDON REFLEXES, HYPOACTIVE 205
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◆ Eaton-Lambert syndrome. This disorder
produces generalized hypoactive DTRs. Early
signs include difficulty rising from a chair,
climbing stairs, and walking. The patient may
complain of achiness, paresthesia, and muscle
weakness that’s most severe in the morning.
Weakness improves with mild exercise and
worsens with strenuous exercise.
◆ Guillain-Barré syndrome. This disorder
causes bilateral hypoactive DTRs that progress
from hypotonia to areflexia in several days.
Guillain-Barré syndrome typically causes muscle weakness that begins in the legs and then
extends to the arms and, possibly, to the trunk
and neck muscles. Occasionally, weakness may
progress to total paralysis. Other signs and
symptoms include cranial nerve palsies, pain,
paresthesia, and signs of brief autonomic
dysfunction, such as sinus tachycardia or bradycardia, flushing, fluctuating blood pressure, and
anhidrosis or episodic diaphoresis.
Usually, muscle weakness and hypoactive
DTRs peak in severity within 10 to 14 days; then
symptoms begin to clear. However, in severe
cases, residual hypoactive DTRs and motor
weakness may persist.
◆ Peripheral neuropathy. Characteristic of
end-stage diabetes mellitus, renal failure, and
alcoholism, and as an adverse effect of various
medications, peripheral neuropathy results in
progressive hypoactive DTRs. Other effects include motor weakness, sensory loss, paresthesia, tremors and, possibly, signs of autonomic
dysfunction, such as orthostatic hypotension
and incontinence.
◆ Polymyositis. In this disorder, hypoactive
DTRs accompany muscle weakness, pain, stiffness, spasms and, possibly, increased size or atrophy. These effects are usually temporary; their
location varies with the affected muscles.
◆ Spinal cord lesions. Spinal cord injury or
complete transection produces spinal shock, resulting in hypoactive DTRs (areflexia) below the
level of the lesion. Associated signs and symptoms include quadriplegia or paraplegia, flaccidity, loss of sensation below the level of the lesion, and dry, pale skin. Also characteristic are
urine retention with overflow incontinence, hypoactive bowel sounds, constipation, and genital reflex loss. Hypoactive DTRs and flaccidity
are usually transient; reflex activity may return
within several weeks.
◆ Syringomyelia. Permanent bilateral hypoac-
tive DTRs occur early in this slowly progressive
disorder. Other signs and symptoms are muscle
weakness and atrophy; loss of sensation usually
extending in a capelike fashion over the arms,
shoulders, neck, back, and occasionally the
legs; deep, boring pain (despite analgesia) in the
limbs; and signs of brain stem involvement
(nystagmus, facial numbness, unilateral vocal
cord paralysis or weakness, and unilateral
tongue atrophy). Syringomyelia is more common in males than in females.
◆ Tabes dorsalis. This progressive disorder re-
sults in bilateral hypoactive DTRs in the legs
and occasionally the arms. Associated signs and
symptoms include sharp pain and paresthesia of
the legs, face, or trunk; visceral pain with retching and vomiting; sensory loss in the legs;
ataxic gait with a positive Romberg’s sign; urine
retention and urinary incontinence; and
arthropathies.
O
THER CAUSES
◆ Drugs. Barbiturates and paralyzing drugs,
such as pancuronium, may cause hypoactive
DTRs.
S
PECIAL CONSIDERATIONS
Help the patient perform his daily activities. Try
to strike a balance between promoting independence and ensuring his safety. Encourage him to
walk with assistance. Make sure personal care
articles are within easy reach, and provide an
obstacle-free course from his bed to the bathroom.
If the patient has sensory deficits, protect him
from injury from heat, cold, or pressure. Test his
bath water, and reposition him frequently, ensuring a soft, smooth bed surface. Keep his skin
clean and dry to prevent breakdown. Perform or
encourage range-of-motion exercises. Also encourage a balanced diet with plenty of protein
and adequate hydration.
P
EDIATRIC POINTERS
Hypoactive DTRs commonly occur in children
with muscular dystrophy, Friedreich’s ataxia,
syringomyelia, or a spinal cord injury. They
also accompany progressive muscular atrophy, which affects preschoolers and
adolescents.
Use distraction techniques to test DTRs; assess motor function by watching the infant or
child at play.
206 DEPRESSION
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Depression
Depression is a mood disturbance characterized
by feelings of sadness, despair, and loss of interest or pleasure in activities. These feelings
may be accompanied by somatic complaints,
such as changes in appetite, sleep disturbances,
restlessness or lethargy, and decreased concentration. The patient also may have thoughts of
death, suicide, or injuring herself.
Clinical depression must be distinguished
from “the blues,” periodic bouts of dysphoria
that are less persistent and severe than the
clinical disorder. The criterion for major depression is one or more episodes of depressed
mood, or decreased interest or ability to take
pleasure in all or most activities, lasting at
least 2 weeks.
Major depression strikes 10% to 15% of
adults, affecting all racial, ethnic, age, and socioeconomic groups. It’s twice as common in
women as in men and is especially prevalent
among adolescents. Depression has numerous
causes, including genetic and family history,
medical and psychiatric disorders, and the use
of certain drugs. It can also occur in the postpartum period. A complete psychiatric and
physical examination should be conducted to
exclude possible medical causes.
H
ISTORY AND PHYSICAL
EXAMINATION
During the examination, determine how the patient feels about herself, her family, and her environment. Your goal is to explore the nature of
her depression, the extent to which other factors affect it, and her coping mechanisms and
their effectiveness. Begin by asking what’s bothering her. How does her current mood differ
from her usual mood? Then ask her to describe
the way she feels about herself. What are her
plans and dreams? How realistic are they? Is
she generally satisfied with what she has accomplished in her work, relationships, and other interests? Ask about changes in her social
interactions, sleep patterns, appetite, normal
activities, or ability to make decisions and
concentrate. Determine patterns of drug and alcohol use. Listen for clues that she may be
suicidal. (See Suicide: Caring for the high-risk
patient.)
Ask the patient about her family—its patterns of interaction and characteristic responses to success and failure. What part does
she feel she plays in her family life? Find out if
other family members have been depressed
and whether anyone important to her has
been sick or has died in the past year. Finally,
ask the patient about her environment. Has
her lifestyle changed in the past month? Six
months? Year? When she’s feeling blue, where
does she go and what does she do to feel better? Find out how she feels about her role in
the community and the resources that are
available to her. Try to determine if she has an
adequate support network to help her cope
with her depression.
CULTURAL CUE Patients who don’t speak
English fluently may have difficulty communicating their feelings and thoughts. Consider using someone outside the family as an interpreter
to allow the patient to express her feelings more
freely.
M
EDICAL CAUSES
◆ Organic disorders. Various organic disor-
ders and chronic illnesses produce mild, moderate, or severe depression. Among these are
metabolic and endocrine disorders, such as hypothyroidism, hyperthyroidism, and diabetes;
infectious diseases, such as influenza, hepatitis,
and encephalitis; degenerative diseases, such as
Alzheimer’s disease, multiple sclerosis, and
multi-infarct dementia; and neoplastic disorders
such as cancer.
◆ Psychiatric disorders. Affective disorders
are typically characterized by abrupt mood
swings from depression to elation (mania) or by
prolonged episodes of either mood. In fact, severe depression may last for weeks. More moderate depression occurs in cyclothymic disorders and usually alternates with moderate
mania. Moderate depression that’s more or less
constant over a 2-year period typically results
from dysthymic disorders. Also, chronic anxiety
disorders, such as panic and obsessivecompulsive disorder, may be accompanied by
depression.
O
THER CAUSES
◆ Alcohol abuse. Long-term alcohol use, in-
toxication, or withdrawal commonly produces
depression.
◆ Drugs. Various drugs cause depression as an
adverse effect. Among the more common are
barbiturates, chemotherapeutic drugs such as
asparaginase, anticonvulsants such as diazepam, and antiarrhythmics such as disopyramide. Other depression-inducing drugs include
centrally acting antihypertensives, such as reserpine (common with high doses), methyldopa,
Suicide: Caring for the high-risk patient
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DEPRESSION 207
One of the most common factors contributing
to suicide is hopelessness, an emotion that
many depressed patients experience. As a
result, you’ll need to regularly assess a depressed patient for suicidal tendencies.
The patient may provide specific clues
about her intentions. For example, you may
notice her talking frequently about death or
the futility of life, concealing potentially harmful items (such as knives and belts), hoarding
medications, giving away personal belongings,
or getting her legal and financial affairs in
order. If you suspect that a patient is suicidal,
follow these guidelines:
◆ First, try to determine the patient’s suicide
potential. Find out how upset she is. Does she
have a simple, straightforward suicide plan
that’s likely to succeed? Does she have a
strong support system (family, friends, a therapist)? A patient with low to moderate suicide
potential is noticeably depressed but has a
support system. She may have thoughts of suicide, but no specific plan. A patient with high
and clonidine; beta-adrenergic blockers such as
propranolol; indomethacin; cycloserine; corticosteroids; and hormonal contraceptives.
◆ Postpartum period. Although its cause
hasn’t been determined, postpartum depression
occurs in about 10% to 20% of women who
have given birth. Symptoms range from mild
postpartum blues to an intense, suicidal, depressive psychosis.
S
PECIAL CONSIDERATIONS
Caring for a depressed patient takes time, tact,
and energy. It also requires an awareness of
your own vulnerability to feelings of despair that
can stem from interacting with a depressed patient. Help the patient set realistic goals; encourage her to promote feelings of self-worth by expressing her opinions and making decisions. Try
to determine her suicide potential, and take
steps to help ensure her safety. The patient may
require close surveillance to prevent a suicide
attempt.
Make sure the patient receives adequate
nourishment and rest, and keep her environment free from stress and excessive stimulation.
Arrange for ordered diagnostic tests to determine if her depression has an organic cause,
and administer prescribed drugs. Also arrange
suicide potential feels profoundly hopeless
and has a minimal or no support system. She
thinks about suicide frequently and has a plan
that’s likely to succeed.
◆ Next, observe precautions. Ensure the pa-
tient’s safety by removing any objects she could
use to harm herself, such as knives, scissors,
razors, belts, electric cords, shoelaces, and
drugs. Know her whereabouts and what she’s
doing at all times; this may require one-on-one
surveillance and placing the patient in a room
that’s close to your station. Always have someone accompany her when she leaves the unit.
◆ Be alert for in-hospital suicide attempts,
which typically occur when there’s a low staffto-patient ratio—for example, between shifts,
during evening and night shifts, or when a critical event such as a code draws attention
away from the patient.
◆ Finally, arrange for follow-up counseling.
Recognize suicidal ideation and behavior as a
desperate cry for help. Contact a mental health
professional for a referral.
for follow-up counseling, or contact a mental
health professional for a referral.
P
EDIATRIC POINTERS
Because emotional lability is normal in adolescence, depression can be difficult to assess and
diagnose in teenagers. Clues to underlying depression may include somatic complaints, sexual promiscuity, poor grades, and abuse of alcohol or drugs.
Use of a family systems model usually helps
determine the cause of depression in adolescents. Once family roles are determined, family
therapy or group therapy with peers may help
the patient overcome her depression. In severe
cases, an antidepressant may be required.
G
ERIATRIC POINTERS
Many elderly patients have physical complaints,
somatic complaints, agitation, or changes in intellectual functioning (memory impairment),
making the diagnosis of depression difficult in
these patients. Depressed older adults who are
age 85 and older, have low self-esteem, and
need to be in control have the highest risk of
suicide. Even a frail nursing home resident with
these characteristics may have the strength to
kill herself.
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