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Vol 27, No. 1, FEBRUARY 2007 http://ccn.aacnjournals.org
Denise M. Lemke has 27 years of experience as a staff nurse in a neurological intensive care
unit, as a neurosurgical coordinator, as a nurse practitioner in neurosurgery, as a nurse
practitioner in interventional neuroradiology, and currently as a neurocritical care nurse
practitioner in the department of neurology. She has a special interest in traumatic brain
injury and its sequelae. She speaks locally and nationally on topics related to neuroscience
and has published articles in SCI Nursing, Journal of Neuroscience Nursing, Advance
for Nurse Practitioners, and Infusion Nursing.
Corresponding author: Denise M. Lemke, Department of Neurology, Medical College of Wisconsin, 9200 W
Wisconsin Ave, Milwaukee, WI 53033 (e-mail: firstname.lastname@example.org).
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
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been associated not only with trau-
matic injuries but also with tumors,
medications have been used to treat
such episodes, although no defini-
tive treatment protocol exists.
Signs and symptoms of sympa-
thetic storming include posturing,
dystonia, hypertension, tachycardia,
pupillary dilatation, diaphoresis,
hyperthermia, and tachypnea.
The episodes appear unprovoked and
can last for hours or end abruptly.
Sympathetic storming often occurs
after discontinuation of administra-
tion of sedatives and narcotics in the
intensive care unit (ICU).
article reviews the pathophysiology
of sympathetic storming, variations
in signs and symptoms, potential
treatment options, and education of
patients’ families and concludes with
a case report.
Sympathetic storming is theo-
rized to be an increase in activity of
the sympathetic nervous system cre-
ated by a disassociation or loss of
balance between the sympathetic
and parasympathetic nervous systems
Theories on the specific
mechanism of dysfunction include
Denise M. Lemke, MSN, APNP-BC, CNRN
Brain injury is one of the most
common types of traumatic injury.
In critical care units, patients with
moderate to severe brain injury are
often intubated and sedated in an
effort to diminish the workload of
the brain. Agitation or restlessness is
common in these patients and can
be associated with fever, posturing,
tachycardia, hypertension, and
diaphoresis. This exaggerated stress
response, known as sympathetic storm-
ing, occurs in 15% to 33% of patients
with severe traumatic brain injury
who are comatose (score on Glasgow
coma scale [GCS] ≤ 8). Sympathetic
storming can occur within the first
24 hours after injury or up to weeks
The precise mechanism for
the increase in activity of the sympa-
thetic nervous system is unknown,
but the increased activity is thought
to be a stage of recovery from severe
traumatic brain injury.
Terms used to describe this phe-
nomenon in published reports
autonomic instability with
Sympathetic storming has
After Severe Traumatic
* This article has been designated for CE credit.
A closed-book, multiple-choice examination
follows this article, which tests your knowledge
of the following objectives:
1. Identify the causes of agitation in brain-
2. Describe the pathophysiological process of
3. Discuss the current medical management
pertaining to sympathetic storming
loss of cortical control,
tion of autonomic balance,
disruption of relay mechanisms.
Sympathetic activity elicits an
adrenergic receptor interaction that
can be inhibitory or excitatory. The
specific response of the target organ
is determined by the category of epi-
nephrine or norepinephrine receptor
, and β
) being stimulated
Normally the parasympa-
thetic nervous system dampens the
effects of increased activity of the
sympathetic nervous system and
returns the body
not occur and the
individual is in
state of stress.
ing a patient into a state of agitation,
extreme posturing/dystonia, tachy-
cardia, tachypnea, hypertension, dif-
fuse diaphoresis, and hyperthermia
within seconds. Signs and symptoms
vary from episode to episode and
from individual to individual.
Baguley et al
suggest that these
episodes have 3 different phases.
During phase 1, which lasts about a
week, patients are asymptomatic
while sedated or receiving paralytic
agents. In phase 2, episodes of sym-
pathetic storming occur with a mean
duration of 74 days after injury. The
end of this phase is defined by the
cessation of diaphoresis. In phase 3,
no further episodes of persistent
dystonia or spasms occur. Because
discontinuation of sedatives and
narcotics is a common trigger, one
could speculate that the episodes
have only 2 phases and that the seda-
tives and narcotics were effectively
preventing the episodes in what
Baguley et al called phase 1.
Triggers, events that immediately
precede an episode, may include
suctioning, repositioning, environ-
mental sensory stimulation (alarms,
equipment), or fever.
of a trigger allows the patient to be
pretreated in an effort to reduce the
length of the episode, lessen its
intensity, or even abort the episode.
defined storming as a
diagnosis of exclusion in patients
who had recurrent spontaneous
episodes of tachycardia, hyperten-
sion, and hyperthermia. Baguley et al
required that 5 of 7 clinical features
(tachycardia, hypertension, tachyp-
nea, hyperthermia, dystonia, postur-
ing, and diaphoresis) be present
Vol 27, No. 1, FEBRUARY 2007 31
Table 1 Effects of the parasympathetic nervous system and the sympathetic
Glycogen to glucose
Decreased cardiac output and
Decreased urinary output;
Decreased motility of stomach
and gastrointestinal tract;
Release epinephrine and
Increased contraction and heart
rate; increased cardiac output
Increased urinary output;
Increased motility of stomach
and gastrointestinal tract;
Table 2 Sympathetic (adrenergic) receptor interactions
Heart, fat cells, kidneys,
brain (posterior lobe of
Heart, fat cells, kidneys
Increases heart rate,
increases cardiac output
and force of contraction,
lipolysis, release of renin,
release of antidiuretic
stomach, liver or
Relaxation of smooth
glucose production and
insulin release, contrac-
tion of skeletal muscle
Vol 27, No. 1, FEBRUARY 2007 http://ccn.aacnjournals.org
before storming could be diagnosed.
For diagnosis of sympathetic storming,
Blackman et al
required that signs and
symptoms occur a minimum of 1 cycle
per day for 3 consecutive days in a
patient with severe brain injury (level
on Ranchos Los Amigos Scale ≤ IV;
Table 3). Symptoms include body
temperature of 38.5ºC or greater,
systolic blood pressure greater than
140 mm Hg, pulse rate of at least 130
beats per minute, respiratory rate of
at least 20 breaths per minute, agita-
tion, diaphoresis, and dystonia.
Documentation of elevated serum
levels of epinephrine or catecholamines
(sampling needed before and during
episode) can confirm the suspicion of
sympathetic storming, although the
diagnosis is generally based on clinical
examination only. No specific location
of injury or pattern of neuronal injury
is apparent on radiographs, although
sympathetic storming is more common
in patients with diffuse axonal injury.
Seizures were once considered a poten-
tial cause of sympathetic storming.
Do et al,
however, reported a case
study in which electroencephalogra-
phy (EEG) was performed on a patient
and theta waves
form, thus con-
firming that the
that can confirm
the diagnosis of
storming are not available, further
investigation into the origin of these
episodes is required.
indicate an acute change in neurolog-
ical status related to an intracranial
source (new or expanding lesion or
deep vein thrombosis or pulmonary
neuroleptic malignant syndrome,
and drug or alcohol with-
Careful assessment is needed
to determine the appropriate workup.
Potential Adverse Effects of
Untreated Sympathetic Storms
Untreated sympathetic storming
increases the risk of secondary injury
to the brain.
Decreases in cerebral
tissue oxygenation occur as a result
of the physiological impact on the
body’s systems. Prolonged hyperten-
sion, arrhythmias, hyperglycemia,
hyperthermia due to elevated meta-
bolic rate, and hypernatremia from
severe diaphoresis occur as a result
of the sympathetic storm.
If the patient sustains uncon-
trolled hyperventilation, decreases
in cerebral oxygenation occur
because of vasoconstriction. During
acute episodes, intravenous admin-
istration of sedatives or narcotics
can provide immediate relief if the
patient is receiving mechanical ven-
tilation. In patients who are not
receiving mechanical ventilation,
additional dosing with enteric oxy-
codone or intravenous morphine
can be used to abort the episode if
care is taken to protect the airway.
Hypertension and arrhythmias
are associated with storming
episodes. Prolonged hypertension
increases the risk of secondary
injury of the brain due to increased
blood flow leading to edema, risk of
rebleeding, and potential cardiac
dysfunction related to prolonged
stress on the heart. In general, acute
hypertension is not treated because
it is a compensatory response. If per-
sistent hypertension is noted, the
degree of treatment or whether anti-
hypertensive medications are insti-
tuted depends on the physician.
Generally, long-term antihyperten-
sive therapy is not needed.
Common arrhythmias include
bradycardia, ectopic beats and irreg-
ular rates, atrial fibrillation, and
Ectopic beats may be multifocal,
preventricular, or nodal in origin.
Ectopic beats, bradycardia, and
irregular heart rates in patients with
traumatic brain injury are generally
not associated with clinical signs of
mias require treatment only if they
are symptomatic or life threatening
(eg, supraventricular tachycardia,
increases in sympathetic activity
also place patients at risk for myocar-
Table 3 Ranchos Los Amigos scale
No response to visual, verbal, tactile, auditory,
Purposeful and appropriate
Purposeful and appropriate (standby assistance
Purposeful and appropriate (modified independent)
necrosis of the
heart have been
occur if circulat-
shifts that over-
load the pul-
Signs and symp-
toms of neuro-
edema are simi-
lar to those for
can be differen-
tiated radiographically. In general,
radiographic changes in neurogenic
pulmonary edema are located from
mid-lung to apex rather than in the
base of the lungs, as noted in adult
respiratory distress syndrome.
Increased metabolic rate elevates
core body temperature, elevates
blood sugar level, and increases the
risk of muscle wasting and weight
loss. In patients with traumatic brain
injury, the most common cause of
hyperthermia is infection. Fever
workup and maintenance of normo-
thermia are essential. Blood sugar
levels should be tightly controlled by
using a sliding scale for insulin or an
insulin infusion to maintain normal
levels. Increased metabolic rate and
diaphoresis can lead to hyperna-
tremia, renal insufficiency, and thick-
ening of pulmonary secretions. A
dietary consultation is important to
determine the patient’s requirements
for energy and free water and to
maintain appropriate levels. Careful
monitoring of weight, input and
output, serial measurements of
serum levels of sodium, glucose, crea-
tinine, and blood urea nitrogen, and
findings on chest radiographs are
necessary to prevent associated
problems (muscle wasting, pressure
sores and decubitus ulcers, renal
failure, atelectasis, and pneumonia).
Medical management of sympa-
thetic storming focuses on treating
the signs and symptoms in order to
reduce the potential adverse effects
of prolonged activity of the sympa-
thetic nervous system. The choice of
medications depends on the practi-
tioner, and an effective dose is often
defined through trial and error. Fre-
quent adjustments may be required
to provide adequate control of signs
and symptoms. Medications that
depress the central nervous system,
thus suppressing the sympathetic
nervous system, are most commonly
used. Opiate receptor agonists,
dopamine agonists, β-blockers, α-
blockers, γ-aminobutyric acid
(GABA) agonists, and sedatives all
have been used (Table 4).
In the ICU, intravenous medica-
tions (eg, morphine, fentanyl, mida-
zolam) are first-line drugs used to
Vol 27, No. 1, FEBRUARY 2007 33
Table 4 Medications used to treat sympathetic storming
Nonselective β agonist
Seizures, use caution in
patients with renal or
caution in patients
with asthma or
Abbreviation: GABA, γ-aminobutyric acid.
Vol 27, No. 1, FEBRUARY 2007 http://ccn.aacnjournals.org
control these episodes. Although
intravenous medications offer rapid
control, dosing can be extreme,
thus placing the patient at greater
risk for respiratory depression.
Enteric medications are added to
facilitate long-term management
of signs and symptoms.
A frequently used medication
regimen is bromocriptine and oxy-
Bromocriptine, a dopamine
receptor agonist, acts at the hypo-
thalamic level, lowering the temper-
ature threshold, diminishing
diaphoresis, and lowering the blood
Dosing starts at 2.5 to
5 mg every 8 hours and may be
adjusted up to 30 or 40 mg daily.
Oxycodone, an opiate agonist, also
has demonstrated effectiveness in
dosing provides a steady serum level
and can begin with 5 mg every 4
hours. Supplemental oxycodone
may be required, and an order for
an additional 5 mg every 4 hours as
needed is recommended. If multiple
additional doses are required, the
dose can be increased to 10 mg every
4 hours. Medications containing
acetaminophen should be avoided
to diminish the risk of acetamino-
If the episodes are associated
with severe hypertension and tachy-
cardia, or if oxycodone and bromo-
criptine do not provide control,
β-blockers and an α-blocker can be
Propranolol, a nonselective
β-blocker, dampens sympathetic
activity, thus slowing neuronal activ-
It also decreases serum levels
and inhibits central fevers
by acting directly within the central
Dosing starts at 10
mg twice a day and is adjusted upward
with doses as high as 640 mg per day
Bradycardia and hypoten-
sion can occur with propranolol.
Caution is advised in patients with
asthma or bronchial disease.
If propranolol is ineffective,
clonidine or labetalol can be added.
Clonidine, an α
-blocker, lowers cir-
culating levels of norepinephrine
and epinephrine, and labetalol acts
as a β
-, and α
Extreme hyperthermia can be
treated with chlorpromazine, a
dopamine antagonist, that can be
given intravenously, intramuscularly,
or enterically to reduce the core tem-
in low doses suppresses hypothala-
mic vasomotor tone, which reduces
body temperature and blocks pilo-
Given the anticholinergic
activity of this medication and the
risk of extrapyramidal effects, long-
term use is not recommended.
Acetaminophen and hypothermia
blankets are used in conjunction
with chlorpromazine to control
body temperature. Hyperthermia
prolongs episodes of storming; thus
maintaining normothermia may
lessen frequency or severity of
episodes. Fever workup is necessary
to rule out meningitis, pneumonia,
urinary tract infections, and deep
Dantrolene is added if contrac-
tures or persistent dystonia are
Dantrolene suppresses the
release of calcium, thus promoting
relaxation of skeletal muscle, which
may help to control hyperthermia.
Dantrolene can reduce somatosym-
pathetic spinal reflex activity, which
would in turn have an inhibitory
effect on overall sympathetic activity.
Other medications have been
reported to treat the symptoms of
sympathetic storming. Baclofen, a
GABA-B agonist, has been success-
fully used intrathecally to control the
episodes, although the precise mech-
anism is unknown.
route reduced the sedation associ-
ated with enteric baclofen but
required surgical placement of the
pump. Its use has been limited to
Scott et al,
in a single study,
reported success of carbidopa/
levodopa, a dopamine agonist, in
treating autonomic dysfunction in a
patient with “locked-in” syndrome.
Cyclopropyl derivatives of oxymor-
phone (naltrexone) can assist in the
control of sympathetic storming.
Medications with inconsistent or no
response include antiepileptic drugs
(phenytoin, phenobarbital, and car-
any medication that suppresses
activity of the sympathetic nervous
system can be used.
Education of Patients’ Families
The patient’s family may perceive
the abrupt onset of sympathetic
storming as a sign of worsening clin-
ical status. Care must be taken to
assure the family that sympathetic
storming can be a normal result of
brain injury. Ideally the family should
be educated before they witness an
episode. An educational tool (Table 5)
would be helpful for preparing
patients’ families. Correct terminol-
ogy should be used with explanations.
The sheet should review pathophysi-
ology, methods of diagnosis, treat-
ment, and ways for family members
The informed family can alert
nursing staff to the episodes, provide
tips to identify triggers, and assist
the heathcare team with treatment.
When the episodes occur, family
members can use cool cloths, mas-
sage, quiet conversation, and sooth-
ing music. These activities provide
the family with a means to help pro-
vide care for the patient and lessen
the inevitable feelings of helplessness
experienced by families dealing with
traumatic brain injury. The follow-
ing case report provides an overview
of the acute management of a patient
with sympathetic storming.
Scott, a 24-year-old man, was an
unrestrained driver in a motor vehi-
cle accident that required prolonged
extrication. At the scene, his pupils
were fixed and dilated. His GCS
score was 5 (eye opening = 1, verbal
responsiveness = 1, motor respon-
siveness = 3), as demonstrated by no
eye opening or speech and weak
mixed posturing. He was intubated
in the field. In the emergency depart-
ment, Scott was intermittently local-
izing to painful stimuli, pupils were
equal and reactive, there was no eye
opening or speech, and his GCS
score was 7 (eye opening = 1, verbal
responsiveness = 1, motor respon-
siveness = 5). An initial computed
tomography scan showed a large
right-sided subdural hematoma with
a significant shift from right to left.
He was taken to the operating room
for emergent evacuation of the sub-
dural hematoma and placement of
an intracranial pressure monitoring
bolt. Intracranial pressure range was
from 5 to 40 mm Hg, with a rapid
increase in pressure with any activity
and a fever spike to 39.4ºC on the
evening of admission.
An intravenous infusion of mida-
zolam was started (2-4 mg/h) with
fentanyl 25 to 50 μg administered
intravenously every hour as needed
Vol 27, No. 1, FEBRUARY 2007 35
Your brain has 2 centers called the
sympathetic (your “get up and go” system)
parasympathetic (your relaxation system)
tems that keep your body at a steady level of functioning (homeostasis). When there is stress, the
system releases chemi-
cals that provide the body with the needed support to respond to the stress. This is called your ”fight or flight” response.
The body’s response to sympathetic release of chemicals:
Increase in heart rate (tachycardia)
Increase in blood pressure (hypertension)
Elevation of temperature (hyperthermia)
Increase in breathing rate (tachypnea)
Increase in muscle tone (dystonia)
Slowing of bowel and bladder activity
system is responsible for “calming” this response and returning you to a normal state of homeostasis.
Occasionally in individuals who suffer traumatic injury to the brain, there may be episodes when the individual appears to be having a
stress response. The heart will race, breathing becomes rapid and shallow, muscles become tight and rigid, they will sweat profusely,
their temperature shoots up, and they look very uncomfortable or “stressed.” There is not a clear explanation for these episodes, but it is
thought that the
system overreacts, leading to a stress response; there is a lack of response of the
to return to a normal state of homeostasis, or a combination of the two.
These episodes can occur without warning or appear to occur spontaneously. The symptoms, as well as the duration of the episode, can
be unpredictable. That is why the nurses refer to this abnormal stress response as
monly appears as medications used to sedate and control pain are discontinued.
Treatment is aimed at controlling the symptoms, decreasing the frequency of the episodes, or stopping the episodes. The nurses will
also try to identify “triggers” or activities that cause an episode. By identifying a trigger, the nurse can pretreat the individual before the
activity or attempt to avoid the activity.
These episodes may start after your family member has been transferred to the general neurological ward. The episodes do not warrant
return to the intensive care unit (ICU). The storming episodes can generally be controlled with careful adjustment of medications and
care aimed at “calming” the storm. The medications used are aimed at slowing the
response or acting as the
Family can help by helping to identify triggers, alerting the nursing staff when an episode occurs, and providing calming activities (mas-
sage, relaxing music, conversation, placing cool cloths on the family member’s forehead). If any of these activities cause an episode,
they should be avoided. Identifying the right combination of medications and activities that help “tone” down the episodes takes time.
Medications and activities need to be adjusted on the basis of your family member’s response to the treatment. Generally over time the
systems return to normal or a modified state and the medications can be slowly discontinued.
© Froedtert Memorial Lutheran Hospital, Inc. 2005. All rights reserved. Used by permission.
Table 5 Educational tool for sympathetic storming
Vol 27, No. 1, FEBRUARY 2007 http://ccn.aacnjournals.org
for treatment of spikes in intracranial
pressure. Findings on neurological
examination remained unchanged
with a GCS score of 6. Within 48
hours, the intracranial pressure had
stabilized. At this time, Scott’s neu-
rological status fluctuated from a
GCS score of 7 (localizing ) to a GCS
score of 8 (following commands).
The monitoring of intracranial pres-
sure and the midazolam infusion
Scott was having nonstimu-
lated episodes of tachycardia (120-
150/min), hypertension (150-210/
80-110 mm Hg), increased posturing,
and diaphoresis consistent with
sympathetic storming. Increased
heart rate and blood pressure
responded temporarily to high
doses of intravenous fentanyl as
needed (1300 μg/24 h) and midazo-
lam (35 mg/24 h).
Storming episodes continued
and administration of 12.5 mg of
metoprolol twice daily was started.
A magnetic resonance imaging study
on day 3 showed a small amount of
bleeding in the left frontal area,
ischemic changes in basal ganglia
on both sides, and ischemic lesions
in the occipital lobe on both sides.
An EEG showed diffuse intermittent
slowing (greater on left side than
right) and no epileptic activity. No
improvement was noted with admin-
istration of metoprolol. As a result,
clonidine 0.1 mg twice daily was
added on hospital day 4.
A tracheostomy was performed
on hospital day 6, and Scott was then
weaned off of ventilatory support
without difficulty. He followed com-
mands intermittently but continued
to have the storming episodes. Fen-
tanyl as needed (625 μg/24 h) and
midazolam (10 mg/24 h) lessened
the response, although nurses
observed that the effect was transient.
Even though the EEG did not show
epileptic activity, the team thought
that silent seizures could not be
ruled out, and phenytoin was started
at 150 mg twice a day. Clonidine was
increased to 0.1 mg 3 times a day
and 5 to 10 mg of oxycodone was
given every 4 hours as needed.
Scott’s family was initially dis-
traught over the storming episodes,
which escalated when he was trans-
ferred to the general neurological
ward. Frequent updates were pro-
vided to discuss the cause of the
episodes, medication changes, the
frequency of episodes, alternative
treatments, and Scott’s response to
treatment. His family was encour-
aged to assist in the monitoring of
episodes and in the use of calming
techniques and cooling baths.
On day 8 after the injury, Scott was
transferred to the general neurologi-
cal ward after he was successfully
weaned off of mechanical ventilator
support. Upon transfer, the meto-
prolol dosage was increased to 25 mg
twice daily, and the bromocriptine
dosage was increased to 5 mg every
8 hours. The evening after transfer,
Scott had a prolonged storming
episode during which the nursing
staff was able to provide only momen-
tary relief with positioning, a cooling
mattress, acetaminophen, and sup-
plemental oxycodone. The episode
was aborted after 10 mg intramuscu-
lar morphine sulfate was adminis-
tered (per physician’s order).
The rehabilitation service was
consulted, and their recommendation
was to increase the dose of bromocrip-
tine to 10 mg every 8 hours and to
discontinue the metoprolol while
adding 20 mg of propranolol twice
daily. At that time, Scott was having
daily temperature spikes (39.7ºC to
40.2ºC), which appeared to aggravate
the storming episodes. Cultures were
negative for bacterial infection, and
a chest radiograph showed no find-
ings indicative of pneumonia or con-
solidation. Acetaminophen was used
in conjunction with a cooling blan-
ket to treat the temperature spikes.
The storming episodes continued,
although they were less frequent and
shorter than before. On day 13 after
the injury, the dosage of propranolol
was increased to 20 mg every 8 hours.
Scott continued to follow com-
mands intermittently (he stuck out
his tongue on command and
squeezed, grasped, and released his
left hand). He was able to track the
individuals in his environment. He
exhibited increased flexor tone in his
left upper extremity and increased
extensor tone in his right upper
extremity. His pupils were equal and
reactive to light and, although he
opened his eyes spontaneously, he
made no attempts to speak. His GCS
score was 11 (eye opening = 4, verbal
responsiveness = 1, motor respon-
siveness = 6). The storming episodes
appeared to have stabilized by this
time, and Scott was transferred to a
subacute rehabilitation facility on
day 21 after injury.
At 7-month follow-up, Scott
remained in the subacute facility.
Neurological examination showed
him to be alert with a flat affect, ori-
ented times 4 with poor short-term
memory and fluent speech. He fol-
lowed commands and moved all 4
extremities (strength grade right 4/5;
left 3/5; he remained wheelchair-
dependent because of coordination
deficits). Scott also exhibited a total
homonymous hemianopic defect on
the left side and a partial homony-
mous hemianopic defect on the right
side. His score on the Glasgow Out-
come Scale was 3 (conscious but dis-
abled/dependent for daily support).
No further storming episodes had
been noted and current medications
included methylphenidate, fluoxe-
tine, and enoxaparin.
Patients with sympathetic storm-
ing must be treated promptly. Intra-
venous medication can provide
immediate control, although the
effect is generally temporary, and
dosing can be extreme, thus placing
the individual at greater risk for res-
piratory depression. These patients
already have significant cerebral
compromise and must be treated
promptly to ensure optimal recovery.
The onset of sympathetic storm-
ing should trigger the institution of
scheduled enteric medications to
provide continuous dampening of
activity of the sympathetic nervous
system. Multiple medications may be
required, as well as a period of trial
and error, before the correct medica-
tion(s) and/or dosages are deter-
mined. An effective starting point is
the use of scheduled oxycodone,
bromocriptine, and if hypertension is
present, propranolol. If hypertension
and other signs and symptoms do
not improve, clonidine can be added
or doses can be adjusted.
The ultimate goal is rapid control
of the signs and symptoms of excess
activity of the sympathetic nervous
system to prevent the secondary
complications of prolonged stress
and to facilitate rehabilitation. Each
case requires individual dosing based
on signs and symptoms and response
to the medication.
The nurse plays a vital role in the
supportive care of patients with a
severe traumatic injury and is a key
player in the diagnosis and manage-
ment of sympathetic storming (espe-
cially in the ICU). Initially the use of
sedatives and narcotics for cerebral
protection can prevent signs and
symptoms of sympathetic storming,
and the onset of episodes frequently
coincides with weaning of patients
off of these medications or with the
discontinuation of these medications.
The nurse can be instrumental in the
coordination of intravenous and
enteric medications, avoiding the
adverse effects of sympathetic
storming, and identifying triggers so
that patients can be transferred to
the general neurological ward.
Long-term use of these medica-
tions is not warranted. Generally
weaning patients off the medications,
one medication at a time, occurs
during the rehabilitation phase. The
precise timing varies, as does the
decision about which medication to
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Vol 27, No. 1, FEBRUARY 2007 37
CE Test Test ID C0712: Sympathetic Storming After Severe Traumatic Brain Injury
Learning objectives: 1. Identify the causes of agitation in brain-injured patients 2. Describe the pathophysiological process of sympathetic storming
3. Discuss the current medical management pertaining to sympathetic storming
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Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. In traumatic brain injuries, agitation and restlessness
can be associated with which of the following?
a. Fever, posturing, and diaphoresis.
b. Seizures, bradycardia, and hypotension
c. Hypertension, tachypnea, and dry skin
d. Bradycardia, hypertension, and seizures
2. Which of the following have been associated with sympathetic storming?
a. Tumors and subarachnoid hemorrhage
b. Diffuse axonal injury and arteriovenous malformation
c. Subdural hemorrhages and stroke
d. Diffuse axonal injury and tumors
3. When does sympathetic storming most often occur?
a. After administering premedication for nausea and phytoin
b. After a craniotomy for evacuation of the hemorrhage
c. After discontinuing sedatives and narcotics
d. After discontinuing antiepileptic medications
4. Which of the following best describes the pathophysiology of
a. An increase in sympathetic responses in the brain creating faster synapse
b. A decrease in the sympathetic responses in the brain creating disassociation
between synapse rates
c. Altered levels of dopamine creating excitatory responses
d. A disassociation between the sympathetic and parasympathetic nervous system
5. The end of a phase 2 episode is defined by which of the following?
a. When seizures are controlled for 6 months
b. Cessation of diaphoresis
c. When follow-up magnetic resonance imaging shows complete resolution of
d. When no further dystonia or spasms occur
6. Which of the following best describes the diagnosis of sympathetic
a. Temperature of 37.5°C, systolic blood pressure less than 145 mm Hg, and
b. Temperature of 38.5°C, diastolic blood pressure less than 80 mm Hg, and
c. Systolic blood pressure greater than 140 mm Hg, agitation, and diaphoresis
d. Systolic blood pressure less than 140 mm Hg, heart rate of at least 120 beats
per minute, and dystonia
7. Prolonged hypertension should be treated because of which
of the following?
a. Increased blood flow and edema, risk of rebleeding, and potential for
cardiac dysfunction related to stress on heart
b. Increased metabolism, cardiac dysfunction and arrhythmias, and loss of
c. Decreased blood flow and edema, agitation, and pain control
d. Cardiac arrhythmias, increased risk of seizures, and risk of rebleeding
8. Differentiation of neurogenic versus pulmonary edema is
confirmed by which of the following radiographic changes?
a. Neurogenic pulmonary edema is noted in lung bases
b. Neurogenic pulmonary edema is noted in mid-lung to apex
c. Pulmonary edema is noted in the mid-lung to apex
d. Pulmonary edema is noted throughout the entire lung fields
9. Which of the following are considered first-line intravenous
medications for sympathetic storm episodes?
a. Midazolam, morphine sulfate, and phenytoin
b. Fentanyl, lorazepam, and haloperidol
c. Lorazepam, morphine sulfate, and haloperidol
d. Morphine, fentanyl, and midazolam
10. Which of the following medications can be added to the
treatment regime for persistent dystonia or contractures if
acetaminophen and cooling do not help for hyperthermia?
a. Dantrolene c. Levodopa
b. Phenobarbital d. Midazolam
11. When is the appropriate time to educate families on
a. Before a witnessed episode
b. Never because families should never witness an episode
c. After the episode has ended
d. 24 hours after an episode, and wait for them to ask the questions
12. Critical care nurse can be instrumental in the supportive care of
patients with a severe traumatic injury in which of the following ways?
a. Coordinating rehabilitation facilities, educating families of rehabilitation
options, and coordinating intravenous and enteric medications
b. Developing a strict care plan to follow and identifying family psychosocial
issues as well as sympathetic storm triggers of the patient
c. Ensuring proper therapies are being done, identifying triggers to transfer
patient to acute ward, and providing frequent medication schedules
d. Coordinating intravenous medications and identifying triggers so that
patients can be transferred to the acute ward
Mail this entire page to:
Aliso Viejo, CA 92656
Test ID: C0712 Form expires: February 1, 2009 Contact hours: 1.0 Fee: $10 Passing score: 9 correct (75%) Category: A Test writer: Todd M. Grivetti, RN, BSN, CCRN
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