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Sympathetic Storming After Severe Traumatic Brain Injury


Abstract and Figures

Patients with sympathetic storming must be treated promptly. Intravenous medication can provide immediate control, although the effect is generally temporary, and dosing can be extreme, thus placing the individual at greater risk for respiratory depression. These patients already have significant cerebral compromise and must be treated promptly to ensure optimal recovery. The onset of sympathetic storming 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 medication(s) and/or dosages are determined. 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 management of sympathetic storming (especially 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 medications 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 eliminate first.
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Vol 27, No. 1, FEBRUARY 2007
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:
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Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail,
been associated not only with trau-
matic injuries but also with tumors,
7, 9
and sub-
arachnoid hemorrhage.
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
(Table 1).
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
include dysautonomia,
autonomic instability with
paroxysmal sympathetic
7, 8
autonomic dysfunction
and diencephalic
Sympathetic storming has
Sympathetic Storming
After Severe Traumatic
Brain Injury
* 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-
injured patients
2. Describe the pathophysiological process of
sympathetic storming
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
, α
, β
, and β
) being stimulated
(Table 2).
Normally the parasympa-
thetic nervous system dampens the
effects of increased activity of the
sympathetic nervous system and
returns the body
to homeostasis.
In sympathetic
storming, this
feedback does
not occur and the
individual is in
an uncontrolled
state of stress.
Episodes are
frequently unpro-
voked, catapult-
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.
Differential Diagnosis
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
nervous system
Glycogen to glucose
Adrenal gland
Decreased cardiac output and
heart rate
Bronchial constriction
Muscular relaxation
Decreased urinary output;
sphincter contraction
Decreased motility of stomach
and gastrointestinal tract;
decreased secretions
Release epinephrine and
Increased contraction and heart
rate; increased cardiac output
Bronchial dilatation
Muscular contraction
Increased urinary output;
sphincter relaxation
Increased motility of stomach
and gastrointestinal tract;
increased secretions
No involvement
No involvement
Table 2 Sympathetic (adrenergic) receptor interactions
Nerve endings,
No interaction
lowers blood
Heart, fat cells, kidneys,
brain (posterior lobe of
pituitary gland)
Heart, fat cells, kidneys
Increases heart rate,
increases cardiac output
and force of contraction,
increased conduction,
lipolysis, release of renin,
release of antidiuretic
No interaction
Lungs, arterioles,
stomach, liver or
pancreas, uterus,
skeletal muscle
Relaxation of smooth
muscle (vasodilatation,
constipation), increased
glucose production and
insulin release, contrac-
tion of skeletal muscle
End effect
Smooth muscle,
Smooth muscle
elevated blood
decreased ability
to defecate
and/or urinate
Vol 27, No. 1, FEBRUARY 2007
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
experiencing an
episode. The
initial EEG
showed delta
and theta waves
without any
epileptic wave-
form, thus con-
firming that the
episode was
unrelated to
seizure activity.
Even though
diagnostic tests
that can confirm
the diagnosis of
storming are not available, further
investigation into the origin of these
episodes is required.
Episodes can
indicate an acute change in neurolog-
ical status related to an intracranial
source (new or expanding lesion or
thyroid storming,
deep vein thrombosis or pulmonary
infectious processes,
neuroleptic malignant syndrome,
malignant hyperthermia,
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
supraventricular tachycardia.
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
hemodynamic instability.
mias require treatment only if they
are symptomatic or life threatening
(eg, supraventricular tachycardia,
atrial fibrillation).
increases in sympathetic activity
also place patients at risk for myocar-
dial infarction.
Myocytolysis and
Table 3 Ranchos Los Amigos scale
No response to visual, verbal, tactile, auditory,
noxious stimuli
Generalized response
Localized response
Purposeful and appropriate
Purposeful and appropriate (standby assistance
on request)
Purposeful and appropriate (modified independent)
contraction band
necrosis of the
heart have been
reported on
autopsy in
patients with
severe traumatic
brain injury.
edema may
occur if circulat-
ing catechola-
mines cause
massive fluid
shifts that over-
load the pul-
monary system.
Signs and symp-
toms of neuro-
genic pulmonary
edema are simi-
lar to those for
adult respira-
tory distress
syndrome but
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
Morphine sulfate,
fentanyl, oxycodone
Midazolam, diazepam,
Baclofen (oral/intrathecal)
Opiate agonist
Dopamine agonist
Nonselective β-
adrenergic antagonist
-adrenergic agonist
Nonselective β agonist
GABA-A agonist
GABA-B agonist
Dopamine antagonist
Common use
Lactation suppression,
infertility, prolactin-
secreting pituitary
Parkinson disease
Malignant hyperthermia
Muscle relaxation
Adverse effect/
Seizures, use caution in
patients with renal or
hepatic disease
Hypotension, use
caution in patients
with asthma or
bronchial disease
Sedation, lowers
seizure threshold,
extrapyramidal side
Hepatic disease
Abbreviation: GABA, γ-aminobutyric acid.
Vol 27, No. 1, FEBRUARY 2007
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
treating episodes.
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-
phen overdosing.
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
of catecholamines,
reduces cardiac
and inhibits central fevers
by acting directly within the central
nervous system.
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
-, 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-
perature rapidly.
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
vein thrombosis.
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.
The intrathecal
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-
and β
(metoprolol, atenolol).
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
to assist.
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.
Case Study
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)
and the
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)
Pupils dilate
Sweating (diaphoresis)
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
neuro storming
sympathetic storming.
It com-
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
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
were discontinued.
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
eliminate first.
1. Kishner S, Augustin J, Strum S. Post head
injury autonomic complications. Available
Accessed November 8, 2006.
2. Thorley RR, Wertsch JJ, Klingbeil GE. Acute
hypothalamic instability in traumatic brain
injury: a case report. Arch Phys Med Rehabil.
3. Baguley IJ, Cameron ID, Green AM, Slewa-
Youman S, Marosszeky JE, Gurka JA. Phar-
macological management of dysautonomia
following traumatic brain injury. Brain Inj.
4. Baguley IJ, Nicholls IL, Felmingham K,
Crooks J, Gurka JA, Wade LD. Dysautono-
mia after traumatic brain injury: a forgotten
syndrome? J Neurol Neurosurg Psychiatry.
5. Cuny E, Richer E, Castel JP. Dysautonomia
syndrome in the acute recovery phase after
traumatic brain injury: relief with intrathecal
baclofen therapy. Brain Inj. 2001;15:917-925.
6. Blackman JA, Patrick PD, Buck ML, Rust
RS. Paroxysmal autonomic instability with
dystonia after brain injury. Arch Neurol.
7. Boeve B, Wijdicka E, Benarroch E, Schmidt
K. Paroxysmal sympathetic storms (dien-
cephalic seizures) after diffuse axonal head
injury. Mayo Clin Proc. 1998;732:148-152.
8. Do D, Sheen VL, Bromfield E. Treatment of
paroxysmal sympathetic storm with
labetalol. J Neurol Neurosurg Psychiatry.
9. Scott JS, Ockey RR, Holmes GE, Varghese G.
Autonomic dysfunction associated with
locked-in syndrome in a child. Am J Phys
Med Rehabil. 1997;76:200-203.
10. Macmillin CSA, Grant IS, Andrews PJD.
Pulmonary and cardiac sequelae of sub-
arachnoid hemorrhage: time for active man-
agement? Intensive Care Med. 2002;28:
11. Russo RN, O’Flaherty S. Bromocriptine for
the management of autonomic dysfunction
after severe traumatic brain injury. J Paedi-
atr Child Health. 2000;36:283-285.
12. Sahr YL, Ghosen I, Vincent JL. Cardiac
manifestations after subarachnoid hemor-
rhage: a systematic review of the literature.
Prog Cardiovasc Dis. 2002;45:67-80.
13. Lemke DM. Riding out the storm: sympa-
thetic storming after traumatic brain injury.
J Neurosci Nurs. 2003;36:4-9.
14. Francois B, Vacher P, Roustan J. Intrathecal
baclofen after traumatic brain injury: early
treatment using a new technique to prevent
spasticity. J Trauma Inj Infect Crit Care. 2000;
15. Meythaler JM, Peduzzi JD, Eleftheriou E,
Novack TA. Current concepts: diffuse axonal
injury–associated traumatic brain injury.
Arch Phys Med Rehabil. 2001;2:1461-1471.
16. Stanford GG. The stress response to trauma
and critical illness. Crit Care Nurs Clin North
Am. 1994;6:693-702.
17. King ML, Lichtman SW, Seliger G, Ehert
FA, Steinberg JS. Heart-rate variability in
chronic traumatic brain injury. Brain Inj.
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
sympathetic storming?
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
sympathetic storming?
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
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... 24 These signs and symptoms vary from episode to episode, as well as from individual to individual. 6 The interruption of diaphoresis is used as a mark between the second and third phases, frequently occurring on the 74 th day after the brain injury. 9 When an episode of mixed PSH occurs, the symptoms manifested are miosis, tearing, bradycardia, bradypnea, hypotension, hypothermia, tidal breathing, and yawning. ...
... 16 In the ICU, intravenous drugs such as morphine, fentanyl and midazolam are the first line of treatment. 6 Morphine, an opioid agonist, performs analgesia and alters the extreme changes of the ANS, as well as dystonia by suppressing the sympathetic flow. 9 Sedatives such as dexmedetomidine and propofol are used to manage episodes of PSH in the ICU. ...
... When treated incorrectly, PSH leads to an increased risk of secondary brain injury. 6 The high adrenergic activity of PSH 4 in association with several episodes of the phenomenon can result in secondary morbidities such as elevated intracranial pressure, cardiac injury, metabolic disorders, 19 systemic abnormalities throughout the body, and increased mortality. 21 A hypermetabolic state during sympathetic hyperactivity can reduce body weight by 25% during just one episode. ...
Full-text available
The present literature review aims to present the physiology of paroxysmal sympathetic hyperactivity (PSH) as well as its clinical course, conceptualizing them, and establishing its diagnosis and treatment. Paroxysmal sympathetic hyperactivity is a rare syndrome, which often presents after an acute traumatic brain injury. Characterized by a hyperactivity of the sympathetic nervous system, when diagnosed in its pure form, its symptomatologic presentation is through tachycardia, tachypnea, hyperthermia, hypertension, dystonia, and sialorrhea. The treatment of PSH is basically pharmacological, using central nervous system suppressors; however, the nonmedication approach is closely associated with a reduction in external stimuli, such as visual and auditory stimuli. Mismanagement can lead to the development of serious cardiovascular and diencephalic complications, and the need for neurosurgeons and neurointensivists to know about PSH is evident in order to provide a fast and accurate treatment of this syndrome.
... To our knowledge, patients with PSH had a more difficult clinical course in rehabilitation and might have more need for feeding and breathing devices, which could result in complications such as infections, which lead to death directly or indirectly. 46,47 In this study, we combined the data of only 2 studies for mortality, and more research is needed to explore this result. The present study has several limitations. ...
Introduction Paroxysmal sympathetic hyperactivity (PSH) is a syndrome of excessive sympathetic activity, mainly occurring in severe traumatic brain injury. However, few studies have reported the actual frequency of PSH and its related risk factors in adult patients with brain injury. Methods We performed this systematic review and meta-analysis to estimate the combined incidence of PSH and the associated risk factors in adult patients with brain injury. This study was registered with PROSPERO international prospective register of systematic reviews (https://www.crd.york. CRD 42021260493), and a systematic search was conducted in the scientific database particularly Embase, PubMed, Web of Science, Cochrane Library, and Google scholar. All identified observational studies regarding the incidence and risk factors of PSH in the adult patient with brain injury were included. Two authors extracted data independently; data were analyzed by STATA Version 16 statistical software. Results The search yielded nine studies involving 1643 adult patients. PSH was detected in 438 patients. The combined incidence of PSH in adult brain injury patients was 27.4% (95% CI: 0.190-0.358). The risk factors include patients’ age (SMD=-0.592, I² =77.5%, 95% CI -1.027– -0.156, P=0.008), traffic accident (OR=1.783, I² =18.0%, 95% CI 1.128–2.820, P=0.013), admission GCS score (SMD=-1.097, I² =28.3%, 95% CI -1.500– -0.693, P=0.000), hydrocephalus (OR=3.936, I² =67.9%, 95% CI 1.144–13.540, P=0.030), and diffuse axonal injury (OR=4.747, I² =71.1%, 95% CI: 1.221–18.463, P=0.025) and were significantly associated with the present of PSH after brain injury . Conclusion PSH occurs in nearly a quarter of the adult patients with brain injury, patient’s age, traffic accident, admission GCS score, hydrocephalus, and DAI were risk factors to PSH in adult patients with brain injury. These findings may contribute to novel strategies for early diagnosis and interventions that aid in the rehabilitation of brain injury patients.
... Electrophysiological investigations of this phenomenon did not show electroencephalographic activity. Many names were attributed to this syndrome: dysautonomia, sympathetic storming, brainstem attack, autonomic dysregulation, and paroxysmal autonomic instability with dystonia [2][3][4][5]. In 2014, the International Brain Injury Association convened a consensus workgroup to clarify its nomenclature and diagnostic criteria. ...
Full-text available
Introduction: Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Methods: We searched MEDLINE, ResearchGate, and Google Scholar, for keywords related to PSH and the role of beta-blockers in moderate-to-severe TBI on September 23, 2020. Two authors blindly screened the articles found with Rayyan. Both resolved their conflicts by mutual consent. If no solution was found, a third author was consulted. Simple descriptive data analysis was performed and the results were presented both in a narrative and tabular form. Results: Of the 19 items found, 10 met the criteria for inclusion. 50% were systematic reviews without meta-analysis, 40% were observational studies, and 10% were experimental studies. Propranolol was the main beta-blocker found in 80% of the studies and was the only molecule used in the treatment of paroxysmal sympathetic hyperactivity in 40% of the included studies. Only two studies evaluated and showed a significant association between beta-blockers and mortality rate (5.1% vs. 10.8%; P=0.03), (3% vs. 15%; P=0.002), respectively. Conclusion: Propranolol is the beta-blocker that has been shown to be effective in reducing the length of stay and mortality rate in moderate-severe traumatic brain injury patients with PSH. However, further studies are needed to precisely define the terms and conditions of its use.
Full-text available
Background: Minor head injury is a nervous system disorder caused by a violent blow or jolt to the head or body. As a consequence of this accident an individual will be losing his awareness signed by headache and pain. One way to overcome it is by giving nursing actions like slow deep breathing therapy.Purpose: getting the effect of slow deep breathing therapy to decrease the pain of minor head injury patient.Metode: this study was a quasi-experimental design with Pretest–posttest design with control group approach. A group of 40 respondents were recruited applying by consecutive sampling technique. The study was conducted between the period of June 25 to July 25 of 2007. The study instrument used a pain scale named NRS (numerical rating scale).Result: Based on the data presented that adult age group of intervention group was 60%, while in control group was 55%. Most of gender category was male, 70% of intervention and 75% of control group respectively. The result of paired samples t-test exam 1 received value sig.(2-tailed) = 0,000, it means that there was different of mean average of pre-test post-test group. Meanwhile, paired samples t-test exam 2 resulted value sig.(2-tailed) = 0,021 (sig>0,05), it means that there was different of mean average of pre-test post-test group.Conclusion: There was effect of slow deep breathing to decrease the pain of minor head injury patient.
Full-text available
The incidence of fractures is the highest prevalence in the world. Fractures by accidents require serious management to prevent serious injuries. The improper first treatment of fracture victims can lead to death and disability. The causes of fractures in Indonesia include traffic accidents. The number of motorized vehicles in Indonesia is increasing by 119.560 cases every year which caused new problems, including security, safety, and traffic congestion. Online motorcycle taxis are alternative public transportation because they can reach places that are not passed by other public transportation. Online motorcycle taxis riders are people who are often on the road and often see even as victims of broken bones from traffic accidents, so there is a need for counseling and handling emergency conditions for motorcycle taxi drivers on the road. This community service activity aimed to increase the ojol drivers’ knowledge and ability in dealing with emergency fractures on the road using discussion methods. The activity was carried out on Thursday, July 16, 2020, carried out face-to-face in the Sukoharjo Regency pavilion, followed by a number of 20 participants. The result of this activity found an increase in the knowledge of ojol drivers by 40% with posttest results of 80% continued with splint dressing. The results of these activities were followed up by coordination with Gojek for greater community service.
A movement disorder is not just a matter of discomfort or disability. More worrisome is that movement disorders lead to a host of secondary complications. Dystonic involvement of the chest wall, neck, and respiratory muscles may cause acute respiratory compromise requiring mechanical ventilation. Excess (hyperkinetic) movements sustained over a period of time increase the risk of muscle breakdown. If patients experience paroxysmal sympathetic hyperactivity, profound dysautonomia often accompanies the uncontrolled movements. It is therefore necessary to recognize these movements and treat some of them urgently. In this chapter, the clinical semiology of movement disorders seen in intensive care units is described to aid recognition. Moreover, we will discuss when they are relevant for day-to-day critical care management.
Full-text available
INTRODUCTION Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. Our study aims to collate existing evidence of the role of beta-blockers in the treatment of PSH. METHOD We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: paroxysmal sympathetic hyperactivity, traumatic brain injury and beta-blockers. No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected ( authors identification, study type, TBI severity, type of beta-blockers used, the dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale , mortality , morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. RESULTS The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale.. mortality, morbidity and length of stay. CONCLUSION At the end of this scoping review, we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.
Traumatic Brain Injury (TBI) is one of the serious life-threatening condition in trauma victim, and as the major cause of disability and death in adult and children. Subdural hematoma is the most often focal intracranial lesion found, with the incidence of 24% in close head injury cases. Approximatelly 6-24% of Atrial Fibrilation (AF) contributes to ischemic stroke and sudden death because of heart failure. We reported a 63 years old female, diagnosed with subdural hematoma of the right temporoparietal, atrial fibrillation and hypertensive heart disease, who arrivde at the hospital with history of unconsciousness, and severe headache due to motor vehicle accident, and undergone a craniotomy clot evacuation and reposition fixation of the fractured bones. The procedure was performed under general anesthesia, using ETT No 7,5., controlled ventilation. NGT no 16 was inserted for gastric decompression. Two mg of Midazolam and 1,5 mg/KgBW of lidocain given intravenously 3 minutes prior to intubations was used as premedications, 100 μg intravenou Fentanyl,was given as co induction. Induction anesthesia was performed using 100mg propofol and 0,1mg/KgBW vecuronium to facilitate intubations. Maintenance of anesthesia was obtained using O2, N2O, sevoflorane, continuous drip of 100 mg/hour propofol, 6mg/hour vecuronium,and 0,25mg/24hours of digoxin continuous drip was given. The procedure was done in 4 hours. During the operation, haemodynamic remained stable with SBP 130 – 150 mmHg, DBP 70-90 mmHg, HR 90-110 bpm irregular and SaO2 99-100 %. EtCO2 level was 30-33. The patient was not extubated by end of surgery, because ECG monitor showed VES bigemini and rapid ventricular response of AF. The patient was directly transferred to the ICU after the procedure. Decreased in brain tissue oxygenation is the physiological impact of body system. Hypertension, arrhythmia, hyperglycemia, hyperthermia and hypernatremia can occur due to sympathetic storm. The most common arrhythmias that could occur are bradycardia, ectopic beat, irregular beat, atrial fibrillation and supraventricular tachycardia. Arrhythmias due to myocardial infarction or thromboemboli (AF and SVT) must be treated immediately when considered as a life threatening condition which provokes a hemodynamic instability and cerebral hypoxia Optimal pre-operative management including oxygenation, cardiorespiration stabilization, arrhythmia managemen and, adequate fluid status, will improve the outcome.
Full-text available
paroxysmal sympathetic hyperactivity is an unwell known pathology, without a clearly established treatment, we aimed to highlight the role of beta-blockers in the management of this condition
Full-text available
Cardiac injury and pulmonary oedema occurring after acute neurological injury have been recognised for more than a century. Catecholamines, released in massive quantities due to hypothalamic stress from subarachnoid haemorrhage (SAH), result in specific myocardial lesions and hydrostatic pressure injury to the pulmonary capillaries causing neurogenic pulmonary oedema (NPO). The acute, reversible cardiac injury ranges from hypokinesis with a normal cardiac index, to low output cardiac failure. Some patients exhibit both catastrophic cardiac failure and NPO, while others exhibit signs of either one or other, or have subclinical evidence of the same.Hypoxia and hypotension are two of the most important insults which influence outcome after acute brain injury. However, despite this, little attention has hitherto been devoted to prevention and reversal of these potentially catastrophic medical complications which occur in patients with SAH. It is not clear which patients with SAH will develop important cardiac and respiratory complications. An active approach to investigation and organ support could provide a window of opportunity to intervene before significant hypoxia and hypotension develop, potentially reducing adverse consequences for the longterm neurological status of the patient. Indeed, there is an argument for all SAH patients to have echocardiography and continuous monitoring of respiratory rate, pulse oximetry, blood pressure and electrocardiogram. In the event of cardio-respiratory compromise developing i.e. cardiogenic shock and/or NPO, full investigation, attentive monitoring and appropriate intervention are required immediately to optimise cardiorespiratory function and allow subsequent definitive management of the SAH.
Full-text available
Heart-rate variability (HRV), a measure of fluctuation around the mean heart rate, reflects the sympathetic and parasympathetic balance of the autonomic nervous system, and is an excellent technique to study cardiovascular tone in patients with neurological injuries. The purpose of this study was to determine whether abnormal HRV is present in patients with traumatic brain injury (TBI) during the post-acute recovery phase. Using a prospective, case/control design, we performed 24-h ambulatory ECG monitoring in seven TBI patients and in seven controls (C). There was a significant difference in root mean squared successive difference of RR intervals (C 40.4 +/- 10.3, TBI 23.3 +/- 16.5, p = 0.04) between TBI and C. Four patients with TBI (compared to one control) had abnormal standard deviation of the RR interval. When these four patients were compared to their matched controls, significant differences were found in frequency domain measure (In total power: TBI 4.4 +/- 0.9 ms2, C 7.1 +/- 1.4 ms2, In low frequency: TBI 3.3 +/- 1.1 ms2, C 6.4 +/- 1.4 ms2; In high frequency TBI 2.0 +/- 1.0 ms2, C 4.8 +/- 1.3 ms2, all p < 0.05). Thus, abnormalities in both time and frequency domains of HRV are present in TBI during the post-acute recovery phase.
Full-text available
. Acute hypothalamic instability occurs in patients with traumatic brain injury (TBI). It usually occurs in the form of autonomic dysfunction syndrome (also known as diencephalic seizures or paroxysmal sympathetic storms); however, there are other causes of acute hypothalamic instability of which the clinician must be aware. Neuroleptic malignant syndrome, malignant hyperthermia, autonomic dysfunction syndrome, and lethal catatonia are all syndromes that clinically present as signs and symptoms of acute hypothalamic instability. Because of the lethal potential of these syndromes, clinicians who care for patients with TBI must be aware of the various syndromes, their clinical presentation, and their treatment. We present a case of life-threatening acute hypothalamic instability in a patient with TBI.
The stress response is a protective system that defends the body from external and internal threats. When the body is confronted with an over-whelming threat, the response becomes uncontrolled, resulting in damage to the body and frequently death. Knowledge of the strengths and pitfalls of this system is important in understanding the responses of the body to trauma and critical illness.
This is a report of a young boy with the unusual combination of autonomic dysfunction with locked-in syndrome following multiple shunt revisions for hydrocephalus. A review of the literature on autonomic dysfunction syndrome and the complex clinical picture of the combined syndromes in a pediatric patient are discussed. The marked effectiveness of treatment with carbidopa/levodopa over bromocriptine for both syndromes is noted.
We describe a patient with a severe traumatic head injury who exhibited paroxysmal sympathetic storms, similar to those described in "diencephalic seizures." No epileptiform activity was evident on electroencephalography, and therapeutic levels of anticonvulsants failed to alter the spells; however, use of morphine sulfate abolished them. The features of this and several previously reported cases refute the primary roles of the diencephalon and seizures in this syndrome. Rather, in the setting of already compromised autonomic neuronal integrity, subtle fluctuations in intraventricular pressure or activation of reflexes triggered from muscle mechanoreceptors or chemoreceptors during episodes of hypertonia are more likely. "Paroxysmal sympathetic storms," a more appropriate descriptive term for these phenomena, should be recognized; thus, unnecessary diagnostic evaluations can be minimized, and appropriate therapy can be initiated.
To better establish the clinical features, natural history, clinical management, and rehabilitation implications of dysautonomia after traumatic brain injury, and to highlight difficulties with previous nomenclature. Retrospective file review on 35 patients with dysautonomia and 35 sex and Glasgow coma scale score matched controls. Groups were compared on injury details, CT findings, physiological indices, and evidence of infections over the first 28 days after injury, clinical progress, and rehabilitation outcome. the dysautonomia group were significantly worse than the control group on all variables studied except duration of stay in intensive care, the rate of clinically significant infections found, and changes in functional independence measure (FIM) scores. Dysautonomia is a distinct clinical syndrome, associated with severe diffuse axonal injury and preadmission hypoxia. It is associated with a poorer functional outcome; however, both the controls and patients with dysautonomia show a similar magnitude of improvement as measured by changes in FIM scores. It is argued that delayed recognition and treatment of dysautonomia results in a preventable increase in morbidity.
This case report describes a child with severe traumatic brain injury with clinical features of autonomic dysfunction in the immediate post-traumatic period. A history of severe asthma in this child contraindicated the use of beta-blockers, the first line approach, and she was managed with bromocriptine (0.05 mg/kg t.d.s) with good effect.
In the early course of severe head trauma, the clinical value of intrathecal administration of baclofen to reduce autonomic disorders and spasticity has not been established. We studied four patients (Glasgow Coma Scale score 3 or 4) with autonomic disorders and spasticity who failed to respond to conventional treatment during the early course of head injury. Baclofen (25 microg/mL) was infused continuously through an intrathecal catheter inserted at patient bedside and subcutaneously tunneled. When this treatment was successful, the spinal catheter was removed and surgically replaced by another catheter connected to a subcutaneous pump. Clinical follow-up was obtained at 6 months after the head injury. Mean delay for the initiation of intrathecal baclofen was 25 days (range, 21 to 31 days), and optimal dose was 385 +/- 185 microg/day. In all patients, the Ashworth score was consistently reduced (3.5 +/- 0.5 vs. 4.5 +/- 0.5 for upper limbs and 2 +/- 0.5 vs. 4.5 +/- 0.5 for lower limbs), as were both the frequency and intensity of autonomic disorders. The spinal catheters were used during a mean period of 9.5 +/- 1.7 days without complications. All three survivors were equipped with a programmable pump and had a lower Ashworth score at 6 months. Autonomic disorders had disappeared in two patients and remained modest in the remaining patient. Continuous administration of baclofen via the intrathecal route using this new technique seems to reduce autonomic disorders and spasticity during the early course of severe traumatic head injury.