Review Article

Management of
Address correspondence to
Dr Carolin I. Dohle, Burke
Rehabilitation Center, 785
Mamaroneck Avenue,
White Plains, NY 10605,
carolin.dohle@gmail.com.
Relationship Disclosure:
Medical Complications
Dr Dohle and Dr Reding Carolin I. Dohle, MD; Michael J. Reding, MD
report no disclosure.
Unlabeled Use of
Products/Investigational
Use Disclosure: Dr Dohle ABSTRACT
and Dr Reding report no
disclosure.
Medical comorbidities and complications are expected following stroke, traumatic brain
Copyright * 2011, injury, and spinal cord injury. The neurorehabilitation physician’s role is to manage these
American Academy of comorbidities, prevent complications, and serve as a medical and neurologic resource for
Neurology. All rights the patient, family, and neurorehabilitation team. The most common comorbidities are
reserved.
similar to those found in the general population, namely hypertension, dyslipidemia,
diabetes mellitus, and ischemic heart disease. Frequent complications encountered in the
neurorehabilitation unit relate to medication side effects, medical comorbidities, and the
direct effect of the neurologic injury. They include orthostatic hypotension; syncope or
presyncope; cardiac arrhythmia; bowel and bladder dysfunction; seizures; pressure sores;
dysphagia-related pneumonia, dehydration, and malnutrition; venous thromboembo-
lism; falls; and sexual dysfunction. This article discusses strategies for managing comor-
bidities and avoiding complications.

Continuum Lifelong Learning Neurol 2011;17(3):510–529.

THE PHYSICIAN’S ROLE IN and vital signs are important indicators of

NEUROREHABILITATION
The neurorehabilitation physician’s pri-
mary responsibility is to optimize the
patient’s medical, neurologic, and behav-
ioral status. This is best accomplished by
(1) treating and managing comorbidities
that preceded the onset of neurologic
impairment, (2) preventing common com-
plications of neurologic injury, (3) provid-
ing ongoing assessments of the patient’s
progress, and (4) modifying treatments
based on patient response. The physician
may also serve as a neurorehabilitation
researcher, team leader, and medical and
neurologic educational resource for the
patient, family, and neurorehabilitation
team members.
Physician rounds on the rehabilitation
nursing unit are an integral part of as-
sessing the patient’s response to treat-
ment. Nursing reports highlight patient-
specific problems that have arisen. This
information plus direct observation of
the patient’s level of alertness, behavior,
the patient’s progress or of intercurrent
problems. Having physical therapy, oc-
cupational therapy, and speech ther-
apy treatment areas on the nursing unit
rather than on another floor or at a
remote location provides the most effi-
cient means of staff communication.
Nursing staff are available to help thera-
pists with patient care if needed. Nursing
and physician staff can directly observe
patient performance in therapy activi-
ties. This direct and frequent interaction
among therapy, nursing, and physician
staff allows for a true interdisciplinary
approach to neurorehabilitation.1
During daily rounds, the physician
pays close attention to the patient’s medi-
cal issues and assesses the adequacy of
his or her rehabilitative equipment (eg,
Is the wheelchair properly adapted to
the patient’s needs? Are splints and
paretic shoulder support systems in
place? Is the patient’s spasticity ade-
quately managed?).

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 KEY POINTS
Formal weekly conferences with all assure they are appropriate and effec- h The neurorehabilitation
members of the neurorehabilitation team tive in optimizing the patient’s ability to physician’s role is to
are an essential component of patient participate in and benefit from the neu- manage comorbidities
care. These team conferences allow team rorehabilitation programs. The neurore- and prevent
members to communicate patient-specific habilitation physician must continue to complications.
goals and progress or impediments to assume primary responsibility for patient h Daily physician rounds
reaching these goals. Each impediment care. The neurorehabilitation physician, optimize assessment of
(eg, depression, pain, somnolence, fatigue, working with the neurorehabilitation the patient’s response
spasticity, extrapyramidal manifestations, team, observes patient performance on to neurorehabilitation
cardiovascular or respiratory instability) is the nursing unit and in therapy sessions programs.
a target for physician intervention. and is therefore ideally situated to make h Weekly team
Anticipation of expected complica- adjustments in medications to regulate conferences identify
tions is based on the type and extent of heart rate, orthostatic hypotension (OH), problems interfering
the neurologic injury and should prompt pulmonary function, blood glucose, som- with functional
evaluation and intervention to prevent nolence, behavior, and pain. improvement.
their development. Examples of com- The frequency and severity of medi- h Comorbidities are
plications include dysphagia, pneumo- cal complications are related to the related to the etiology
nia, dehydration, malnutrition, pressure severity of neurologic impairment, the of neurologic
sores, bowel and bladder dysfunction, interval following the onset of neuro- impairment.
spasticity, contractures, and depression. logic impairment, and the number and h The neurorehabilitation
Ongoing surveillance of these efforts severity of medical and neurologic co- physician must accept
will document their efficacy or signal the morbidities. Physician practices and care responsibility for the
need to change treatment. settings with patients with severe impair- patient’s overall
Comorbidities are often inherent in ments who have many medical comor- medical management.
the etiology of the neurologic impair- bidities will encounter the most medical Consultants can be
ment. Stroke is a vascular disorder and complications. used to optimize
patient care and
hence carries with it a high frequency of
MANAGEMENT OF COMORBID to help inform and
cardiac, renal, and diabetic comorbidi-
support the
ties. Stroke is also a geriatric disorder CONDITIONS
neurorehabilitation
with associated neurodegenerative, pul- Hypertension and
physician.
monary, gastrointestinal, and musculo- Hyperlipidemia
h The frequency and
skeletal comorbidities. Traumatic brain Hypertension and hyperlipidemia are
severity of medical
injury (TBI) and spinal cord injury (SCI) expected in geriatric neurorehabilitation complications are
are more common in younger, physi- patients, and their effective management related to the severity
cally active individuals who are more is an essential part of American Heart of neurologic
likely to demonstrate risk-seeking be- Association recommendations for second- impairment, the
havior and recreational drug use and to ary stroke prophylaxis.2 In patients on interval following the
have psychosocial comorbidities. the neurorehabilitation unit, labile blood onset of neurologic
Because medical, neurologic, and be- pressure fluctuations are common be- impairment, and the
havioral complications are often predict- cause of exertion, pain, or anxiety. Adjust- number and severity of
able and comorbidities are common, it ing the intensity of exercise, giving pain medical and neurologic
is important for the neurorehabilitation medication prior to exercise, or giving comorbidities.
physician to develop the skill set and anxiolytic medications are all appropriate
confidence necessary for their man- interventions for such patients.
agement. Use of consultants can help
inform and support the neurorehabili- Diabetes
tation physician; however, consultant Diabetic management should target
opinions and advice need to be weighed normal or near-normal blood glucose
by the neurorehabilitation physician to levels. Numerous studies have shown

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 Medical Complications
KEY POINTS
h Euglycemia is the
goal of diabetes
management but
must be balanced
with the risk of
hypoglycemia in
patients unaware
of or unable to
express symptoms of
hypoglycemia.
h Daily physician
assessment of
congestive heart
failure signs and
symptoms plus periodic
$-natriuretic peptide,
blood urea nitrogen/
creatinine, electrolyte,
and chest x-ray provide
guidance in managing
cardiac response to
progressive self-care
and mobility exercises.
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that the better the blood glucose regu-
lation the better the functional out-
come. However, a number of special
issues interfere with diabetic manage-
ment following neurologic injury: inabil-
ity to express hypoglycemic symptoms
because of aphasia, altered awareness of
impending hypoglycemia, dysphagia-
related variability in food intake, and
meals and exercise that are regulated by
the patient’s schedule and not by the
patient. Blood glucose is frequently dif-
ficult to control when the patient is on
tube feedings, and the timing of moni-
toring and insulin administration should
be adjusted. The goal is to balance the
need for near-normal blood glucose
levels with avoidance of symptomatic
hypoglycemia. Because glycosylated
hemoglobin levels change slowly, we
have not found them to be a useful
guide for diabetic management during
the several-week inpatient neurorehabil-
itation stay. Fingerstick blood glucose
determinations before meals and at bed-
time remain the most valid assessment of
diabetic management.
Congestive Heart Failure
American Heart Association standards
for managing congestive heart failure
(CHF) advocate use of three classes of
medication: a diuretic, a beta-blocker,
and an angiotensin-converting enzyme
inhibitor or angiotensin receptor blocker.3
Use of these standard medications may
have to be modified during neuroreha-
bilitation because of dysphagia-related
dehydration, diabetic or vascular renal
insufficiency with hyperkalemia, and bra-
dycardia or OH. Daily rounds by the
physician are important for adjusting dos-
ages of CHF medications. Patients with
dysphagia may not be able to tolerate the
use of diuretic medications. They may
report that they do not like the taste of
thickened liquids and hence cannot main-
tain adequate oral hydration if given a
diuretic. Frequent small amounts of thick-
ened liquid several times per day will help
supplement hydration. It is difficult to
maintain adequate hydration for those on
honey-thick liquids. It is important to note
that diuretics are used to enhance renal
sodium excretion. Extracellular water vol-
ume decreases as a result of enhanced
renal sodium clearance. Coupling a di-
uretic with adequate hydration is neces-
sary to ensure adequate renal function.
On daily rounds the physician can observe
the patient’s resting respiratory rate while
the patient is in a comfortable position
in bed or in a wheelchair. Auscultation of
the lungs with detection of basilar rales,
dullness to percussion over the lung bases,
presence or absence of jugular venous
distension (more than 12 cm above the
sternomanubrial joint is abnormal in
either supine or sitting position), and
presence of either bilateral pedal or pre-
sacral edema are all indicators of CHF.
Daily observation for the presence of
these signs of CHF should trigger further
evaluations such as serum $-natriuretic
peptide (BNP) assessment. BNP is a re-
liable marker of atrial stretch response
to intravascular volume expansion un-
less significant renal dysfunction is pres-
ent. In the presence of chronic kidney
disease with serum creatinine greater
than 2.0 mg/dL, the BNP may not accu-
rately reflect CHF status. A follow-up
chest x-ray can confirm the clinical assess-
ment. Follow-up echocardiograms are
not usually available on the neuroreha-
bilitation unit. With daily physician assess-
ments and appropriately timed serum
BNP, blood urea nitrogen (BUN), serum
creatinine, and serum electrolyte assess-
ments it is usually possible to titrate the
patient’s CHF medications to optimize
functional status and avoid dehydration.
PREVENTION OF COMMON
COMPLICATIONS
Cardiovascular Complications
Orthostatic Hypotension. OH is
defined by the American Academy of
June 2011

Neurology and the Consensus Commit-
tee of the American Autonomic Society
as a drop in systolic blood pressure of
20 mm Hg or more or a drop in diastolic
blood pressure of 10 mm Hg or more.4
OH is common on the neurorehabilita-
tion unit. It is often attributed to over-
aggressive antihypertensive medication
management during the acute hospital
phase of patient care. Blood pressures
seem well managed when patients are
supine in bed, but OH becomes appa-
rent when they begin spending more
time sitting in a wheelchair, standing,
and walking. OH can be a manifestation
of deconditioning, dehydration, or an-
other comorbidity such as diabetic auto-
nomic neuropathy. Dehydration is a
particularly common cause of OH fol-
lowing neurologic injury with dysphagia.
While diuretics are frequently used as
one of the primary medications for hyper-
tension management, dysphagia requiring
use of nectar- or honey-consistency liquids
is an indication of severely compromised
ability to maintain oral hydration. Diu-
retics should be avoided in patients with
dysphagia requiring thickened liquids
unless they are needed for management
of advanced CHF.
SCI is commonly associated with OH
in the acute phase postinjury. OH follow-
ing SCI may persist several weeks into
the chronic phase5,6 and is frequently
asymptomatic.7 OH is particularly severe
in patients with cervical SCI.8 These pa-
tients may require use of a tilt table and
abdominal binder to gradually accom-
modate to the upright posture.
Management of OH includes de-
creasing or stopping antihypertensive
medications, ensuring adequate hydra-
tion with oral fluids if possible or with IV
fluids if needed, applying elastic com-
pression wraps to the lower extremities,
and using an abdominal binder to help
increase peripheral and visceral venous
return. Such treatment is outlined in
Case 6-1. Patients should be kept out of
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KEY POINT
bed as much as possible and encouraged h Orthostatic hypotension
to sit up or stand as they are able with following stroke or
appropriate monitoring of blood pres- traumatic brain injury
sure. Patients who cannot tolerate being is most commonly due
upright even with the above interven- to antihypertensive
tions may need to practice incremental medication or
habituation to upright posture using a dehydration with
tilt table or a specialized wheelchair that prerenal azotemia
tilts to a recumbent position with elevat- and is particularly
ing leg rests and a fully reclining back severe in patients
with cervical spinal
rest (Figure 6-1). Medical management
cord injury.
may include IV volume expansion and
adding vasoconstrictors such as midro-
drine.9 Observational studies have sup-
ported the use of fludrocortisone.10
Autonomic Dysreflexia. Autonomic
dysreflexia (AD) is defined as significant
hypertension (20 mm Hg to 40 mm Hg
above the patient’s baseline or above
150 mm Hg if baseline is not known)
with altered vasomotor tone (sweating,
piloerection, skin blanching or flushing,
headache, blurred vision, nasal conges-
tion, acute feeling of anxiety or impend-
ing crisis). AD is common following SCI
at or above the T6 level. Susceptibility to
AD begins once the acute spinal shock
phase has passed and tendon hyper-
reflexia becomes manifest. AD may also
occur with minimal symptoms experi-
enced by the patient (silent AD). The
frequency and severity of cardiovascular
dysfunction seem to be directly related
to the severity of the SCI.11 In patients
with a complete lesion above T6, all
hypothalamic and brainstem regulation
of sympathetic innervation to the car-
diovascular system is disrupted, leaving
the parasympathetic system as the only
supraspinal input, which may lead to
bradycardia and arrhythmia. Further,
patients with severe SCI at T6 or above
may experience symptomatic fluctuations
in blood pressure due to decentralization
of vasomotor control. In these patients,
intermittent surges in blood pressure
may occur between hypotensive epi-
sodes.12 Fecal impaction, urinary reten-
tion, urologic or abdominal infection, or
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 Medical Complications

Case 6-1
A 74-year-old man with a history of left basal ganglia infarct resulting in right hemiparesis and dysarthria
was admitted to the neurorehabilitation unit. Review of his hospital chart revealed that the patient had a
history of uncontrolled hypertension, coronary artery disease, diabetes mellitus, and hyperlipidemia. During
his acute hospitalization he had frequent blood pressure spikes with systolic blood pressure recordings of up
to 200. He was being treated with hydralazine, metoprolol, and lisinopril and was on a pureed diet and
nectar-thick liquids because of dysphagia. On his second day of admission, the patient began physical
therapy. He was ambulating 10 feet with moderate assistance at the hemibar when he suddenly became
diaphoretic and weak and reported dizziness. He was immediately placed in a reclining wheelchair and
brought back to his room. His heart rate was 90 beats/min, his blood pressure was 90/68 mm Hg, his oxygen
saturation was 96% breathing room air, and his blood sugar was 114. His morning laboratory results
showed a serum sodium of 147, a blood urea nitrogen of 35, and a creatinine of 1.0. The patient appeared
lethargic. He was placed in Trendelenburg position, and over the next 20 minutes his mental status slowly
returned to baseline. His medications were reviewed and a decision was made to stop his hydralazine.
Because of his history of diabetes and coronary artery disease, the lisinopril and metoprolol were reduced in
dose but not stopped. Orders were given to obtain blood pressure measurements with the patient sitting up
to avoid falsely high readings. Orders were also written to give 3 ounces of nectar-thick fluids with each
therapy session to improve hydration. Elastic wraps and an abdominal binder were applied to further provide
circulatory support. The patient was allowed to return to his therapy sessions after his symptoms subsided.
Comment. This case illustrates that even patients with baseline hypertension and high blood pressure
readings when supine may suffer from orthostatic hypotension when standing or sitting up in a chair.
The doses of blood pressure medications need to be decreased, with an emphasis on those that do not
benefit other medical conditions the patient has. Blood pressure readings for this patient should be
taken in a sitting position. Because he has dysphagia and is taking nectar-thick liquids (which he does not
like), he is having trouble maintaining adequate hydration.

another stimulus to the sacral, lumbar,
or thoracic spinal cord often triggers an
AD episode. Placing the patient in a
FIGURE 6-1 Tilt-in-space wheelchair. These wheelchairs
may be beneficial for patients with
orthostatic hypotension, poor head or trunk
control, and decreased endurance, and can help relieve pain
from pressure ulcers through weight shifting. The angle
between the seat and wheelchair back remains constant
when the patient is tilted back.
seated rather than supine position may
be of immediate benefit. Using lido-
caine gel to ease noxious stimuli asso-
ciated with bladder catheterization or
digital disimpaction may terminate the
episode. The Consortium for Spinal
Cord Medicine clinical practice guide-
lines acknowledge that no randomized
controlled trials to identify optimal med-
ical management of AD have been
reported.13 Reasonable alternatives are
oral nifedipine, hydralazine, prazosin,
captopril, and transdermal nitrate. In
severe persistent episodes, IV nitro-
prusside in an emergency department
or intensive care unit setting may be
required for patient stabilization. Use of
sildenafil for erectile dysfunction within
24 hours is a relative contraindication
for use of nitrates.
Syncope or Presyncope. If a clear
orthostatic association with syncope or
presyncope exists, the etiology of the

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event is clearly related to hypotension.
Time in the wheelchair may also be an
important variable. Vasovagal events
associated with toileting are also com-
mon. Constipation with or without fecal
impaction or functional vesicourethral
outflow obstruction may be precipitat-
ing events and should be treated appro-
priately. Every syncopal or presyncopal
event should be considered as possibly
related to some other etiology unless
the situation and recovery are suffi-
ciently clear. Fingerstick blood glucose,
pulse oxymetry, EKG, and observation
for absence seizure, cryptic seizure, or
another etiology should be considered.
Patients taking multiple antihyperten-
sive medications and those with under-
lying dehydration or vascular volume
contraction may not show a quick return
of blood pressure to baseline level when
placed supine or in Trendelenburg posi-
tion, and supplemental IV hydration may
be needed. Likewise, recovery of base-
line level of alertness may be prolonged
for minutes to an hour. Focal neurologic
findings that had improved since an
initial stroke may worsen and reflect
hypoperfusion of marginally functioning
ischemic stroke penumbra. Modification
of antihypertensive medication may be
needed to allow a slightly higher blood
pressure to maintain perfusion. If symp-
toms persist despite measures to in-
crease cerebral blood flow, follow-up
imaging would be indicated to evaluate
stroke progression versus secondary
hemorrhage into an ischemic stroke.
Transient Arrhythmias. Asymptom-
atic bradycardia or minimally symp-
tomatic bradycardia with fatigue, poor
endurance, or exertional dyspnea is often
observed in patients participating in
physical therapy and occupational ther-
apy programs. If this is attributable to
the use of beta-blockers and the EKG is
unchanged from baseline (except for
heart rate), a reduction in beta-blocker
dosage is indicated. Patients with chronic
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KEY POINTS
stable atrial fibrillation may show occa- h Initial treatment for
sional asymptomatic 2- to 3-second autonomic dysreflexia
pauses between QRS complexes. This is is to place the patient
most common while resting in a wheel- in a seated position,
chair or in bed and resolves with minimal correct obstructive
activity. Reduction in beta-blocker, di- bowel, bladder,
goxin, or calcium channel blocker dosage or other etiologies,
may be sufficient to correct the problem. and then provide
The frequency of such events is easily specific medication
documented on the neurorehabilitation management of
residual hypertension.
unit with Holter monitoring and can help
guide medical management. A system h Assess syncopal or
for urgent cardiology consults should be presyncopal events as
available. Mobitz type II heart block, com- possible cardiac
arrhythmia, cardiac
plete heart block, or bradycardia associ-
ischemia, pulmonary
ated with signs or symptoms of CHF or
embolus, or seizures.
angina pectoris are treated according to
advanced cardiac life support protocol, h Modification of
antihypertensive
and patients with these arrhythmias
medication may be
should be emergently transferred to an
needed to allow a
acute care hospital setting. slightly higher blood
Tachycardia is also commonly noted pressure to
by nursing or therapy staff. EKG con- maintain perfusion.
firmation of sinus tachycardia may in-
dicate hypoglycemia, deconditioning,
dehydration, anemia, withdrawal from
beta-blocker, hyperthyroidism, CHF, or
pulmonary embolism. Each should be
considered and judged according to
physical examination, laboratory results,
chest x-ray, and blood gas findings.
Tachycardia due to deconditioning is a
diagnosis of exclusion. New-onset atrial
fibrillation, often with a heart rate above
150, requires further cardiovascular eval-
uation to exclude acute myocardial is-
chemia, heart failure, hyperthyroidism,
or another etiology. The severity of the
tachycardia, the need for further cardiac
evaluation, the need for repeat neuro-
imaging, and the decision to initiate war-
farin treatment usually warrant transfer
back to an acute care hospital setting.
Seizures
The incidence of seizures within the first
2 weeks of ischemic stroke has been
estimated to be approximately 2% to
23% depending on study design.2 The
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 Medical Complications

KEY POINT
h Routine seizure
prophylaxis is not
recommended for
patients with stroke
or intracerebral
hemorrhage.
incidence of clinical seizures following
intracerebral hemorrhage (ICH) has
been reported to be 14%, with most
occurring at or shortly after the acute
event.14 Electroencephalographic evi-
dence of seizure activity may be as high
as 28% to 31% in patients with ICH
having continuous EEG monitoring. No
clear evidence exists for prophylactic
use of anticonvulsants to improve func-
tional outcome or survival. Patients with
ischemic stroke or ICH who have clini-
cally apparent seizures and patients
with electroencephalographic evidence
of seizures with accompanying change
in mental status should be given anticon-
vulsants. Evidence from animal studies
suggests that phenobarbital, topiramate,
lamotrigine, and phenytoin may impair
motor recovery15; however, clinical evi-
dence is still lacking.
Pressure Sores
Pressure sores are defined as wounds
resulting from pressure or friction on
any part of the body. Immobilized neu-
rorehabilitation patients in hospital
and nursing home settings following
stroke or SCI are at high risk of devel-
oping pressure sores. Pressure sores
can cause pain, increase disability, and
lead to systemic infections and death.16
The incidence of pressure sores is es-
timated to be 25% to 30% in patients
with SCI17,18 and 20% in patients with
stroke.19,20
Pressure ulcers develop when the
pressure on the tissue is persistently
greater than the capillary pressure, which
has been traditionally quoted to be
32 mm Hg, for more than 2 hours.21
However, newer studies have shown that
with increasing external pressure the ar-
teriolar pressure increases through auto-
regulation unless the external pressure
exceeds the diastolic pressure. At this
point, a significant decrease in tissue oxy-
gen partial pressure (PO2) occurs with
resulting tissue hypoxia and necrosis.
Risk factors include compressive
forces and shearing forces.21 Compres-
sive forces are directed perpendicular to
the skin surface, whereas shearing forces
are exerted parallel to the skin surface.
Shearing forces depend on the position
of the patient. The shear exists between
the different layers of the fascia. The in-
fluence of body weight on shearing and
compressive forces is such that in
patients with cachexia higher peak pres-
sures exist than in larger persons, in
whom the pressure is dispersed through-
out a larger surface area.22 The duration
of pressure has been found to be an
independent risk factor, and the fre-
quency of turning the patient has been
linked to the incidence of pressure
ulcers.23 The risk of developing pressure
sores is further increased in patients with
decreased sensitivity to pain from the
pressure and those who have decreased
ability to shift their weight in order to
reduce the pressure.
Poor nutrition is an independent risk
factor for pressure sores. Low albumin
levels have been associated with a higher
risk of developing these lesions. Indi-
viduals who are malnourished have a
twofold to threefold higher risk of devel-
oping ulcers than patients with normal
nutritional status, and providing individ-
uals with nutritional supplements has
been shown to accelerate healing.24 Pa-
tients with albumin levels of less than
3.5 have been shown to have a greater
risk of developing ulcers and slower ul-
cer healing.25
Pressure ulcers develop over bony
protrusions. A study involving patients
with SCI found that the ischial tuber-
osities, sacrum, greater trochanters, lat-
eral malleoli, and heels are commonly
affected.26 Shear forces and inconti-
nence with skin maceration further
traumatize the skin and facilitate bacte-
rial and fungal infections.
The Braden scale and the Norton
scale are used to identify patients at

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risk for developing pressure ulcers. The
Norton scale rates the patient’s physical
condition, mental status, activity, mobil-
ity,andcontinence.TheBradenscalemea-
sures friction, shearing forces, sensory
perception, skin moisture, nutritional in-
take, and physical activity. Both scales
have been shown to have limited inter-
rater reliability and tend to overestimate
the risk of developing pressure sores.27
Preventive measures suggested by
the Consortium for Spinal Cord Injury
include avoidance of prolonged immo-
bilization; daily inspection of skin with
particular attention to coccyx, ischium,
trochanters, and heels because these
areas are at greatest risk for develop-
ment of pressure ulcers; avoidance of
shearing forces; preventing moisture ac-
cumulation; and providing pressure re-
lief support for areas at risk.
Computerized bed mattress systems
are available to attenuate pressure points
and change the patient’s position from
one side to the other (Figure 6-2). Gel
or graduated foam cushions may allevi-
ate pressure when the patient is sitting
up in a wheelchair (Figure 6-3). Fre-
quent weight shifting is also important
for these patients, as well as avoidance
of any pressure points on the paretic
limb by leg rests or foot rests. Pressure
points over the heels can be reduced by
pressure relief ankle-foot orthoses. Ade-
quate intake of calories, protein, micro-
nutrients, and fluid should be provided.
Treatment is based on pressure sore
staging (Table 6-1); an example of ap-
propriate pressure sore treatment is
given in Case 6-2. The ulcer should be
measured with every dressing change,
and good hand hygiene should be en-
sured before and after dressing changes.
Cleaning of the ulcer should be per-
formed with normal saline; solutions
containing alcohol and rubbing of the
wound should be avoided. Stage I ulcers
can be treated with a hydrocolloid dress-
ing. These nonbreathable dressings are
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KEY POINTS
biodegradable and adhere directly to h Preventive measures
the skin, making additional taping un- for pressure sores
necessary. They have to be changed include avoidance
every 3 days or more frequently when of prolonged
excess drainage from the wound occurs. immobilization; daily
For stage II and III ulcers, dressings inspection of skin with
made from sodium carboxymethyl- particular attention
cellulose can be used. These dressings to coccyx, ischium,
form a gel that absorbs wound exudates trochanters, and heels;
and traps bacteria. They may also be avoidance of shearing
forces; preventing
impregnated with silver. Silver ions are
moisture accumulation;
released in the wound and exert an anti-
and providing pressure
microbial effect against a wide range of relief support for areas
bacterial organisms, including vancomycin- at risk.
resistant Enterococcus, methicillin-
h Pressure sore staging
resistant Staphylococcus aureus, and
helps objectify progress
Pseudomonas.28 Collagenase-containing and guide therapeutic
gels can be used for minor debridement interventions.
of the ulcer bed if needed. Surgical de-
bridement is indicated for removal of sig-
nificant necrotic tissue. More advanced
pressure sores, such as stage III and stage
IV, require more intense treatment. The
use of vacuum-assisted closure (VAC)
therapy has been shown to be effective
in these wounds. VAC is safe and easy to
apply and is thought to work by increas-
ing local blood flow to the wound, in-
creasing cell proliferation, and increasing
formation of granulation tissue. These
FIGURE 6-2 Bed with alternating pressure air mattress to
constantly change pressure points. These beds
have multipositional capabilities for additional
relief of possible pressure points.
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 Medical Complications
FIGURE 6-3 Wheelchair cushions. A, gel wheelchair
cushions distribute body weight over the area
of the entire cushion, reducing pressure.
However, they may be quite heavy, do not absorb shocks as well
as other cushions, and have the potential of leaking. B, foam
wheelchair cushions are light and usually easy to maintain.
Several density-graded foams can be used in one cushion to
provide different amounts of support for different skin areas;
however, the foam may lose its shape over time. C, air-inflated
wheelchair cushions are composed of an array of small
interconnected air bladders. Individual air bladders can be tied
off to customize pressure points. These cushions may provide
less stability and are potentially difficult to clean.
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mechanisms promote wound healing
and increase speed of wound closure.
Surgical debridement may be required
prior to using a VAC system whenever
significant necrotic tissue is present.
Surgical closure of the wound by creating
skin flaps is the most aggressive treat-
ment option, but it depends on the pa-
tient’s surgical risk and the prognosis of
the underlying neurologic or medical
disorder.
Dysphagia-Related Complications
Dysphagia and its management are dis-
cussed in detail in the article ‘‘Treatment
of Language, Motor Speech Impairments,
and Dysphagia.’’ The most important
medical complications of dysphagia are
pneumonia, dehydration, malnutrition,
unreliable medication intake, and upper
airway obstruction.
A bedside evaluation of swallowing
should be conducted prior to initiation
of oral intake of food or liquids following
stroke or TBI.29 Based on the bedside
dysphagia evaluation, patients at risk for
aspiration can be given nectar- or honey-
consistency liquids. Patients deemed
unsafe for oral feeding require naso-
gastric feeding tube placement. Naso-
gastric tubes are poorly tolerated by
patients and proper positioning must
be checked by air bolus auscultation
over the abdomen prior to each feed-
ing. If a nasogastric tube is required
for more than 1 or 2 weeks a percuta-
neous endoscopic gastrostomy (PEG)
tube should be placed.
Patients with dysphagia significant
enough to require thickened liquids
are at risk for recurrent aspiration of
saliva and other thin liquids between
meals and at night. Using an oral swab
to cleanse the teeth, tongue, and buc-
colabial folds after meals can help de-
crease the amount of bacterial and
particulate material available for aspira-
tion. Use of incentive spirometry, nebu-
lized bronchodilator treatments, and
June 2011
 KEY POINTS
a h Chemical or surgical
TABLE 6-1 Criteria for Staging of Pressure Ulcers
debridement may
Stage Criteria be necessary to
ensure effective
I Nonblanchable erythema of intact epidermal skin, usually over bony
vacuum-assisted closure
prominence. This is an indication of individuals at risk for developing skin
ulceration. The affected skin can be painful, soft or firm, and may be of pressure sores.
warmer or cooler than the surrounding tissue. h Dysphagia evaluation
II Shiny or dry, shallow superficial ulcer penetrating into the dermal skin and treatment
layer, often with red or pink wound bed. can prevent
III More extensive tissue damage with full-thickness skin loss penetrating dysphagia-related
into the subcutaneous fat tissue layer but not into layers of fascia, complications such
tendon, muscle, or bone. Can present as a deep crater in areas with as pneumonia,
increased adipose tissue but may be shallow in areas without dehydration, and
significant subcutaneous fat. malnutrition.
IV Extensive damage with full-thickness skin loss and involvement of
underlying fascia, tendons, muscle, or bone. Eschar formation may
be present in the wound bed. Ulcers may be shallow in areas without
underlying adipose tissue but can otherwise be very deep.
a
A form of pressure-related injury not included in this staging system is deep tissue injury, which is
an injury to the subcutaneous tissue layers caused by pressure that frequently gives the appearance
of a deep bruise. Such lesions can be recorded as unstagable.

chest percussion and postural drain- with hospital-acquired pneumonia and

age by physical therapists, respiratory
therapists, and nursing staff can also
help mobilize increased tracheobron-
chial mucus formed in response to
chronic low-grade aspiration. Chest aus-
cultation, pulse oximetry, and vital signs
can signal significant change in respira-
tory status prompting an x-ray to eval-
uate for pneumonia. Guidelines out-
lining the antibiotic treatment of adults
health careYacquired pneumonia have
been published by the American Tho-
racic Society and the Infectious Diseases
Society of America.30
Dysphagia significant enough to
require use of thickened liquids places
patients at significant risk of dehydra-
tion. Patients will report that they do not
like thickened liquids and will often
refuse them. Allowing patients access

Case 6-2
A 36-year-old man was admitted to the spinal cord unit 2 weeks after a motorcycle accident. He had
sustained multiple bone fractures, liver and spleen lacerations, and a T8 spinal cord transection. On
examination, the nurse noticed a 4 cm diameter erythematous area over his sacrum that did not blanch
when touched. In the center, a 2 cm diameter shallow ulcer was present. The base of the ulcer was pink
and clean with hair follicles visible. The wound was classified as a stage II pressure ulcer. It was gently
cleaned with normal saline, and a silver impregnated sodium carboxymethylcellulose dressing was
applied. The patient was frequently turned, and pressure on his sacral area was minimized using an
alternating pressure air mattress. While sitting in a wheelchair, he was supported with a gel-based
wheelchair cushion. His wheelchair was placed in a reclining position at regular intervals during the day to
further alleviate any pressure points. The patient’s albumin level was 2.8, so he was started on a
multivitamin, vitamin C, and a protein-enriched diet. With the above measures, his ulcer slowly improved.
Comment. This case illustrates the importance of aggressive management of pressure ulcers. Management
includes wound care, patient positioning, alleviation of pressure points, and nutritional support.

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 Medical Complications
to water, such as with the Frazier Rehab
Institute Free Water Protocol (permit-
ting small sips of water between meals
with nursing staff providing oral and
dental hygiene following each meal),
may be appropriate.31 This allows pa-
tients to safely consume small volumes
of thin liquids and improves hydration.
Diuretics should be stopped unless
needed for management of active CHF.
To ensure adequate hydration, it is rea-
sonable to request that patients receive
at least 3 ounces of thickened liquid with
each therapy session. Renal and electro-
lyte checks can be used to follow the
patient’s response. If necessary, a nurs-
ing order can be written to give the pa-
tient 250 mL of thickened liquid as a
medication every 4 to 6 hours while
awake. Supplemental IV hydration may
also be needed. It is common to monitor
the BUN/creatinine ratio, with values
greater than 20 indicating prerenal
azotemia due to dehydration. Patients
with dysphagia may be sufficiently mal-
nourished so as to show only mildly
elevated BUN/creatinine ratios because
of dietary protein depletion. Such pa-
tients may have elevated serum so-
dium values in the 150 range, serving
as a reliable secondary marker for sig-
nificant dehydration.
Malnutrition due to dysphagia and in-
adequate calorie intake can be followed
using body weight, but values fluctuate
and change slowly. Urinary ketones may
be detectable after a 24-hour fast. Use
of urinary ketone levels as a marker for
inadequate calorie intake is valid even in
patients with diabetes as long as no glyco-
suria is present. Serum prealbumin levels
fall much earlier than serum albumin or
total serum protein levels and are the best
marker for inadequate protein intake.
All patients on an altered-consistency diet
should be assessed for the need for die-
tary supplements and multivitamins.
If the above measures are not effec-
tive in maintaining hydration, nutrition,
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and medication administration, a PEG
tube should be considered. Having nurs-
ing staff estimate the amount of food on
the diet tray that is consumed provides a
reasonable approximation of total calo-
rie consumption. Patients and families
may reject discussions of PEG placement
because they perceive it as artificially pro-
longing life. However, case-matched con-
trolled studies have shown that patients
given PEG tube feedings do as well as
equally severely impaired patients who
do not need PEG feeding.32 They have
similar Functional Independence Mea-
sure efficiency values and are equally
likely to return to their home. PEG feed-
ings allow patients who are effectively
starving to show significant functional re-
covery. Most will not need their PEG
tube for more than 4 to 10 weeks, and
most PEG tubes can be easily removed
by traction or balloon deflation on the
neurorehabilitation unit or in the office.
To prevent spilling of gastric content
to the peritoneum, PEG tubes should
remain in place for at least 2 weeks
prior to removal, with some recom-
mending up to 6 weeks.
Deep Vein Thrombosis
In patients admitted to a rehabilitation
hospital and in patients within 21 days of
stroke onset, the prevalence of deep vein
thrombosis (DVT) has been reported to
be 34% to 40.2% and even as high as
50%.33 The prevalence of DVT in patients
with TBI has been reported to be 11%.34
Most of these patients were asymptom-
atic.35 Higher incidences seem to be re-
lated to greater severity of weakness.36
DVTs usually occur in the paretic leg.
It is important to be vigilant for the
development of DVT in the neurore-
habilitation population because clinical
signs may not be present in these pa-
tients owing to sensory loss and the
inability to report symptoms because
of cognitive or language impairment.
Screening tools should be cost-efficient,
June 2011

noninvasive, easily obtainable, and highly
sensitive and specific. The criterion
standard for diagnosing DVT is contrast
venography; however, this procedure is
invasive and not without risks such as
allergic reaction, nephrotoxicity in pa-
tients with preexisting kidney disease,
and postvenography thrombosis.37 Se-
rum D-dimer levels, which are elevated
in the presence of venous clot formation,
have been evaluated in several studies. In
patients with low clinical suspicion of
DVT, a normal D-dimer serum value can
be used to safely exclude the presence
of DVT.38 Another accepted diagnostic
modality is Doppler ultrasonography,
which is cost-efficient and safe and has
a high sensitivity and specificity (96%
and 98%, respectively). Compressibility
of veins under probe pressure is also
a very accurate test.39 The sensitivity is
best for proximal DVTs and less opti-
mal for isolated calf DVTs.
Prevention of DVT and venous throm-
boembolism ( VTE) is important for pa-
tients with immobilization due to TBI,
SCI, or stroke. Prophylactic use of knee-
or thigh-length graded compression
stockings (GCSs) has been studied, but
their use has not shown a significant
decrease in the incidence of VTE in pa-
tients with stroke.40 One study using
thigh-length GCSs showed no signifi-
cant decrease in the incidence of DVT
after stroke but found that their use was
associated with a significant increase in
superficial skin lesions.41 However, in
studies examining the incidence of DVT
in patients hospitalized for any reason,
the use of GCSs has been shown to be
beneficial.42 Because of the possibility
that they may have some benefit and the
benign nature of their use, GCSs are
used as part of routine DVT/VTE prophy-
laxis in most neurorehabilitation units.
Successful pharmacologic prophy-
laxis with unfractionated heparin (UFH)
has been demonstrated in surgical pa-
tients. In patients with ischemic stroke,
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KEY POINT
prophylaxis with UFH has shown an h In patients with ischemic
almost 80% reduction in the incidence stroke, prophylaxis with
of DVT.43 Low-molecular-weight hepa- unfractionated heparin
rin (LMWH) given once daily has been has shown an almost
found to be at least as effective in pre- 80% reduction in the
venting DVT as UFH given 3 times a incidence of deep
day44 and to be superior to twice daily venous thrombosis.
injections.45 The risk of major adverse
events such as bleeding has been re-
ported as similar or slightly reduced
following the use of LMWH versus
UFH in these trials. LMWH is less likely
than UFH to produce heparin-induced
thrombocytopenia.
Recently published guidelines for
the management of ICH state that ‘‘after
documentation of cessation of bleeding,
low-dose subcutaneous low-molecular-
weight heparin or unfractionated hepa-
rin may be considered for prevention
of VTE in patients with lack of mobility
after 1 to 4 days from [ICH] onset.’’14
This recommendation is listed as Class
IIb, indicating that the benefit may be
greater than the risk based on limited
patient populations studied. The Con-
sortium for Spinal Cord Medicine guide-
lines recommend the use of LMWH
within 72 hours of SCI provided no ac-
tive bleeding is present. They recom-
mend enoxaparin 30 mg subcutaneous
every 12 hours, dalteparin 5000 units
subcutaneous daily, or warfarin to a
therapeutic international normalized
ratio of 2 to 3. DVT prophylaxis for
patients with SCI is recommended for 8
weeks for patients with complete motor
deficits and for 12 weeks for such
patients with other risk factors for VTE
complications. DVT prophylaxis for
patients with stroke and TBI is usually
continued until the patient can ambu-
late distances of 150 feet with or with-
out therapist assistance or until the
patient is sent home or to a custodial
care setting.
Venous compression pump systems
are mostly reserved for patients unable
to take LMWH or UFH because of the
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 Medical Complications

KEY POINT
h Chronic constipation is
expected in immobilized
patients and can
be prevented.
presence of active bleeding, heparin-
induced thrombocytopenia, or other
disorders affecting blood clotting. Foot,
calf, and sequential calf-thigh compres-
sion pump systems are available.
Sequential calf-thigh systems provide
optimal prophylaxis but are poorly
tolerated because of discomfort and
interruption of sleep. Foot-pump sys-
tems are tolerated the best but are not
as effective as either calf or sequential
calf-thigh applications.46 Rapid com-
pression of the venous plexus in the
instep of the foot is able to produce a
100 mm Hg plethysmographically
detectable pulse wave in calf veins.
The pulse wave is thought to provide
venous pulse pressures similar to step-
ping and weight bearing during the
gait cycle; however, these devices are
not frequently used or not used
correctly.
Bowel and Bladder Dysfunction
Colonic stasis is expected as a result of
immobility of any cause. A high-fiber
diet containing 35 grams of fiber plus a
stool softener such as docusate sodium
100 mg 3 times daily is an initial pro-
phylactic option. Use of bisacodyl sup-
positories daily or every other day if no
bowel movement occurs is reasonable.
Manual insertion of the suppository ini-
tiates the anal-colon defecation reflex.
Bisacodyl also has a direct effect on the
smooth muscle of the colon, stimulating
colonic emptying. Additional strategies
such as enemas or lactulose may be
needed. Lactulose can produce loose
stools in any individual if given in higher
doses. Lactulose is not absorbed and is
without systemic toxicity. Polyethylene
glycol compounds (eg, Miralax) may also
be helpful. However, if a patient cannot
move his or her bowels for several days,
the possibility of an obstruction must be
ruled out.
Urinary incontinence (UI) or uri-
nary retention affects a large percent-
age of patients with acquired brain or
spinal cord injury. The prevalence of
UI after stroke has been reported as
almost 50% (including complete and
incomplete UI).47 However, this prev-
alence is linked to the severity of
neurologic injury. Only 5% of patients
with pure motor strokes are expected
to have UI,48 while approximately 75% of
patients with motor, hemisensory, and
hemianopic neurologic impairments are
expected to experience UI during the
first month following stroke. Case 6-3

Case 6-3
A 78-year-old woman with recent infarct involving the left temporal-parietal cortex had resulting global
aphasia and right hemiparesis. On the second day of her admission to the inpatient rehabilitation unit,
the physical therapist noticed that she seemed less alert than on the day of admission and that she
appeared uncomfortable. She was afebrile. Discussion with nursing staff revealed that the patient had
not voided over the past 8 hours. On physical examination, dullness to percussion over the suprapubic
region was present. Bladder scan showed a postvoid residual volume (PVR) of 700 mL. Intermittent
catheterization was initiated, and urine analysis and urine culture were obtained. PVR assessments were
ordered every 6 hours with instructions to perform intermittent catheterization for a PVR volume greater
than 250 mL. Additionally, she was started on tamsulosin for internal urethral sphincter relaxation.
Ciprofloxacin was started subsequently when her urine analysis showed significant pyuria.
Comment. This case illustrates that it is necessary to be vigilant for stroke complications such as
urinary retention because patients often cannot report specific symptoms because of their neurologic
dysfunction. Careful assessment of the patient’s voiding status and frequency of bowel movements
must be made to avoid obstructive uropathy and fecal impactions. Urinary retention is treated with
intermittent catheterization rather than an indwelling catheter.

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gives an example of a patient with
global aphasia with urinary retention
who is unable to verbalize her con-
cerns and has only nonspecific symp-
toms, highlighting the importance of
routinely evaluating patients for the
presence of urinary retention. Patients
with poststroke UI have higher mor-
tality rates than those without UI (60%
versus 20% in one study49 ), and dis-
ability is worse at 3 months in patients
with UI. The natural progression of
poststroke UI is such that most patients
improve.49 Age younger than 75 years
and lacunar infarcts are associated with
significant probability of recovery. UI
following neurologic injury can be due
to either impairment of the bladder’s
ability to store (urge incontinence) or
failure to empty (urinary retention with
overflow incontinence). Stress incon-
tinence is usually caused by lax pu-
dendal musculature due to childbirth
or uterine, vesicle, or rectovesical pro-
lapse and is not a primary sequela of
neurologic injury.
Urinary retention is common (75%
of patients during the first month)
following middle cerebral artery dis-
tribution stroke with hemiparesis and
hemisomatosensory and hemianopic
visual impairments. Bladder emptying
is normally under voluntary control
regulated by the medial frontal cortex
which controls the pontomesence-
phalic reticular formation micturition
center. The pontomesencephalic mic-
turition center coordinates parasympa-
thetic fibers from S2 through S4 that
cause detrusor muscle contraction
and sympathetic fibers from T11 to
L1 that cause relaxation of the internal
urethral sphincter. Overall, activation
of the sympathetic nervous system
leads to urinary continence, while ac-
tivation of the parasympathetic ner-
vous system facilitates voiding. Aware-
ness of bladder volume is mediated by
spinal cord dorsal column propriocep-
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tive afferents projecting to the so-
matosensory cortex of the paracentral
lobule on the medial aspect of the
interhemispheric fissure. During cys-
tometric instillation of carbon dioxide,
the first sensation of bladder fullness
starts at a filling volume of about
125 mL. Voluntary inhibition of voiding
is controlled by the motor cortex in
the paracentral lobule giving rise to
descending efferents in the lateral col-
umns which initiate contraction of the
external urethral sphincter and the
urogenital diaphragm. Voluntary con-
traction of the external sphincter and
urogenital diaphragm results in reflex
inhibition of the detrusor muscle and
inhibition of the urge to void.
Neurologic injuries can impair uri-
nary continence in several ways. Large
middle cerebral artery distribution hemi-
spheric injury may initially cause de-
trusor atony that may last for several
weeks, causing urinary retention requir-
ing intermittent urinary catheterization.
With time such lesions then give rise
to disinhibition of the pontomesence-
phalic micutrition center with detrusor
hyperreflexia and urge incontinence.
Several studies have shown a correla-
tion between frontal lobe lesions and
urinary urge incontinence.50 SCI above
the conus medullaris as well as brain
stem lesions affecting the pontomesen-
cephalic reticular formation can cause
dyssynergia between detrusor muscle
contraction and internal sphincter rel-
axation leading to urinary retention.
With time such SCI lesions may also
give rise to a spastic, hyperreflexic urge-
incontinent bladder.
Urinary tract infections (UTIs) are
common following neurologic injury.
Patients with urinary urgency, frequency,
dysuria, or incontinence should have
a urinalysis with urine culture if indi-
cated. It is important to realize that a
clean voided midstream urine speci-
men is often unobtainable in patients
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 Medical Complications

KEY POINTS
h Intermittent bladder
catheterization is
preferable to
indwelling catheter
for management of
urinary retention.
h Time-prompted
voiding schedules
can ameliorate
urge incontinence.
with neurologic impairments who are
unable to participate in the procedure.
Such patients may need external con-
dom specimens (males) or catheterized
urine specimens (females). Contami-
nation of the urine specimen by vagi-
nal or perineal mucus frequently gives
rise to artifact in laboratory analysis
of pyuria and bacteriuria. Early recog-
nition and treatment of UTI may pre-
vent development of symptomatic in-
fections or urosepsis which can impede
stroke recovery and prolong the hospi-
tal stay.51
Urinary retention is an indepen-
dent risk factor for UTI,52 and if it is
severe enough it may lead to renal in-
sufficiency and renal failure. Indwelling
Foley catheters are one means of treat-
ing urinary retention. They have, how-
ever, been shown to significantly in-
crease the risk of developing a UTI.53
Intermittent catheterization based on
bladder ultrasound determinations every
6 hours is associated with a signifi-
cant decrease in UTIs. The risk of in-
ducing infection versus the need to
prevent bladder distension is probably
optimized by requesting that the pa-
tient be catheterized when postvoid
residual volume by Doppler determi-
nations is in excess of 350 mL. This is
based on the observation that the nor-
mal upper limit of bladder volume is
500 mL for women and 700 mL for men.
Indwelling Foley catheters should be re-
served for patients for whom intermit-
tent catheterization is difficult because
of their size, presence of urethral trauma,
infected sacral sores made worse by in-
continence, or behavioral issues. Anti-
septic Foley catheters as well as cathe-
ters coated with antibiotics suitable for
chronic use have been examined; how-
ever, no good evidence exists regard-
ing their efficacy in preventing UTIs.
Studies examining prophylactic treat-
ment with antibiotics in patients with
indwelling Foley catheters have shown
mixed results. The prophylactic use of
antibiotics carries the risk of selecting
for resistant organisms and is not rec-
ommended. Urinary tract antiseptics
such as methenamine mandelate and
methenamine hippurate, which are con-
centrated in the urine and metabolized
to formaldehyde in an acidic urine, are
bactericidal for all organisms and may
have a limited role in the prevention of
recurrent UTIs in selected patients re-
quiring indwelling Foley or suprapubic
catheters.
Time-prompted voiding schedules
30 minutes after meals and every 2
hours between meals while awake can
decrease urge incontinence. Kegel ex-
ercises are appropriate for women
with comorbid stress incontinence but
have limited use in patients with neu-
rologic injury. Condom catheters are
useful for symptomatic management
of urge incontinence in men without uri-
nary retention.
Pharmacologic treatment of urinary
retention due to internal urethral sphinc-
ter disinhibition can be initiated with !1
receptor antagonists, which exert their
action specifically on !1A receptors in
the prostatic urethra and the vesi-
courethral junction. Such medications
have also shown benefit in women
with urinary retention due to stroke,
TBI, or SCI.54 They are also useful in
men with coexisting prostatic hyper-
trophy. Urecholine may be helpful in
stimulating detrusor contractility but is
relatively contraindicated in patients
with cardiac disease.
Drugs with anticholinergic and anti-
muscarinic effects, such as oxybutynin
and solifenacin, are often used to treat
urge incontinence. They have limited
ability to cross the intact blood-brain
barrier; however, they should be used
with caution in patients with strokes
or other CNS disorders that can inter-
fere with the blood-brain barrier be-
cause they may potentially interfere

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with cognition, memory, and overall
stroke recovery.
Sexual Dysfunction
Stroke may lead to complex issues con-
cerning a patient’s sexuality.55 Altered
self-esteem due to physical dependency
on spousal assistance for self-care func-
tions, depression with loss of libido,
hemiparesis with inability to accom-
modate accustomed sexual positions,
and medication side effects are all rele-
vant contributing factors. Loss of libido
may be due to depression, which is read-
ily treatable. Impotence may be due to
side effects of medications such as anti-
hypertensive agents or due to antide-
pressants themselves. Altered self-esteem
can be addressed by psychological coun-
seling. It is important for the physician
to broach the subject of sexuality with
an open-ended question inviting the
patient’s response, which can be done
when probing for poststroke depres-
sion symptoms.
Sexual dysfunction following TBI
is also common and has been widely
reported.56 TBI is a disorder affecting
younger, more physically active indi-
viduals. Bifrontal involvement may give
rise to inappropriate sexual expres-
sion, pseudobulbar emotional lability
that can interfere with sexual expres-
sion, apathy, and depression. Psycho-
logical counseling for the patient and
his or her partner may help implement
behavior modification techniques. Use
of fluoxetine or sertraline may help
with management of pseudobulbar
affect. Antidepressants that are un-
likely to affect sexual function, such
as mirtazapine and bupropion, can be
recommended.
Surveys of both men and women
with SCI show that sexual function is
lower in priority than concern for mobil-
ity, self-care independence, and bowel
and bladder continence. Reflex erec-
tions in response to manual stimulation
Continuum Lifelong Learning Neurol 2011;17(3):510–529
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KEY POINT
can be achieved by men with complete h Sexual dysfunction
SCI but may require oral sildenafil, may respond to
tadalafil, or vardenafil to allow penetra- elimination of offending
tion. Intraurethral pellet or intracaver- antihypertensive
nous injection of alprostadil can also medication, treatment
be used. Such methods are not likely of depression, and
to produce ejaculation. Semen collec- sexual counseling.
tion for artificial insemination can be
obtained in a fertility clinic with an
anal electrode used to stimulate ejac-
ulation. Women with preservation of
sensitivity in the T11 to L2 dermatomes
may have adequate psychogenic stimu-
lation to provide vaginal lubrication. A
water soluble lubrication jelly can also
be recommended. Obstetrical counsel-
ing concerning the risks of pregnancy
following SCI is appropriate to allow
an informed decision prior to unpro-
tected intercourse. Women with SCI
above T6 are at risk for AD during la-
bor and delivery.
Falls and Fractures
Every patient requiring neurorehabili-
tation is at risk for falls. Use of stan-
dardized falls risk scales such as the
Berg Balance Scale are useful to quan-
tify this risk and help prioritize safety
intervention strategies and equipment.
The Berg Balance Scale assesses bal-
ance in 14 tasks relevant to daily living
such as sitting and standing unsup-
ported, transferring between sitting
and standing, picking up items from
the floor, turning around to look over
shoulders, and reaching forward with
an outstretched arm. Each task is graded
on a 4-point scale.
The neurorehabilitation team should
allow as much independence as pos-
sible without the patient incurring a
significant risk of falling. Patients with
cognitive impairment, impulsivity, dys-
praxia, or mixed expressive-receptive
aphasia may not be able or willing to
cooperate with safety precautions. Bed
or wheelchair alarms, direct nursing
or therapist observation of the patient
www.aan.com/continuum 525
 Medical Complications

KEY POINT
h A risk-benefit
assessment of
fall prevention
strategies should
consider patient
acceptance or rejection
of their use.
when he or she is out of bed, wheel-
chair lap belts, and enclosed bed sys-
tems offer graded interventions to
reduce falls. These safety interventions
may not be tolerated by some patients
and actually increase their risk of fall-
ing if they cause agitation or the patient
struggles against them. Moving the pa-
tient to a private room and having a
family member stay with the patient
is sometimes feasible. Providing indi-
vidual patient supervision is costly but
should be provided if other measures
fail. Psychiatric consultation may be re-
quested when pharmacologic interven-
tion is required to ensure patient safety.
Many neurorehabilitation physicians are
experienced in the use of psychoactive
medications and manage patients who
are agitated or confused without psy-
chiatric consultation.
Special undergarments with impact-
absorbing pads over the greater tro-
chanters may reduce the risk of frac-
tures.57 Patient compliance with their
use is poor because of their bulky ap-
pearance and the mechanics of taking
them on and off while toileting.
Evidence supports the use of bisphos-
phonates in patients following stroke to
prevent fractures.58 Bisphosphonates
are also commonly prescribed following
SCI and in patients with severe TBI and
limited mobility. Use of a calcium sup-
plement with vitamin D is also reason-
able for such patients.59
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