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The ABC’s of Stroke Complications

W. David Freeman, M.D.,1 Steven B. Dawson, M.D.,1 and Kelly D. Flemming, M.D.2


Stroke is the third leading cause of death in the United States, with more
than 140,000 deaths per year. Complications related to stroke resulting in morbidity
and mortality are very common and may result from cerebral and extracerebral causes.
Cerebral causes include cerebral edema, hemorrhagic conversion of an ischemic
infarct, and progression of penumbra to infarction. Extracerebral complications

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include deep vein thrombosis and pulmonary embolism, urinary tract infection, and
aspiration. Many of these complications are largely preventable and often tracked as
‘‘quality metrics’’ in institutions with a stroke center designation. The focus of the
article is primarily on common poststroke complications, such as aspiration, DVT,
decubitus ulcers, seizures, and urinary catheter infections. Knowledge about potential
poststroke complications is critical to earlier diagnosis, proper preventive strategies,
and management.

KEYWORDS: Stroke complications, aspiration, deep vein thrombosis, pneumonia

Stroke-related death 1
and its complications2–26 CEREBRAL COMPLICATIONS OF STROKE
(Fig. 1), can be conceptualized into 2 types: cerebral or
extracerebral (Table 1). Cerebral complications arise Cerebrovascular Pathophysiology
intracranially and occur as part of the subsequent path- An overview of cerebral complications is provided in
ophysiology after the initial stroke, such as a massive Table 1. Ischemia causes brain injury, which manifests as
ischemic stroke leading to swelling, herniation, and neurologic deficits. The type of neurologic deficit de-
brain death. Extracerebral complications after stroke pends on the area of brain affected. Neurons and glia are
are defined by the organ systems affected (e.g., endo- strictly aerobic tissue, with the highest metabolic de-
crinologic, pulmonary, cardiac, gastrointestinal). This mand of all tissues within the human body. The brain
classification of stroke complications is useful, holistic, takes at least 15% of the cardiac output, indicative of its
and helps provide a comprehensive approach in manag- high metabolic demands for oxygen and glucose. Brain
ing stroke patients. tissue without oxygen and glucose quickly depletes intra-
Complications of stroke are largely preventable. cellular ATP and rapidly converts to converting glucose
A simple mnemonic, the ABC’s, can help practitioners to lactate, which produce 2 ATP, compared with up to
remember and treat such complications (Table 2). The 36 ATP from aerobic metabolism. Anaerobic conditions
prevention of these complications is important to re- are intolerable to brain tissue and quickly create an
duce morbidity and mortality from stroke as well and intracellular acidosis, which triggers a cascade of events
serve quality improvement goals. that either lead to programmed cell death, if there are

Department of Neurology, Mayo Clinic, Jacksonville, Florida; Semin Neurol 2010;30:501–510. Copyright # 2010 by Thieme
Department of Neurology, Mayo Clinic, Rochester, Minnesota. Medical Publishers, Inc., 333 Seventh Avenue, New York, NY
Address for correspondence and reprint requests: W. David 10001, USA. Tel: +1(212) 584-4662.
Freeman, M.D., Mayo Clinic, Cannaday 2 East, Jacksonville, FL DOI:
32224 (e-mail: ISSN 0271-8235.
Stroke; Guest Editor, Kelly D. Flemming, M.D.

with a middle cerebral artery occlusion with an area of

potentially viable penumbra has a variable amount of
time before the penumbra becomes completely in-
farcted or irreversible, similar to the core region of
infarction. Several other factors can lead to stroke
progression. The first is the ability of cerebrovascular
collaterals to maintain flow to the area of penumbra.
The second factor is time, which is of the essence, as
some patients have more robust collaterals. A third
factor is the degree of cerebral perfusion pressure (CPP)
which is derived from mean arterial pressure (MAP)
minus intracranial pressure (ICP). Many patients have
Figure 1 Complications after stroke. DVT, deep vein an acute hypertensive response in the setting of an acute
thrombosis; UTI, urinary tract infection. (Modified from stroke. This can be thought of as a somewhat self-
Langhorne P. et al. Stroke 2000; 31:1223–1229).2 protective reflex similar to the Cushing reflex. Hypo-
tension is injurious to ischemic stroke patients due to
this area of vulnerable normal brain tissue. Other
marginal energy/nutrient supply, or cell death in extreme factors include blood rheology, hemoglobin, and oxy-

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metabolic deficits. The region of the brain that receives gen delivery capacity of the blood, abnormal coagula-
less than 10 mL/100 g/min of cerebral blood flow (CBF) tion, or thrombotic potential. Factors within the
will infarct if this is not corrected in minutes. In ischemic vascular wall that contribute to vessel occlusion and
stroke, this area is termed the core region of infarction. ischemic infarction include fatty material within pla-
Brain tissue that receives more than 20 but less than ques causing platelet adhesion, subsequent red clot
50 mL/100 g/min CBF is oligemic or reduced. Oligemic formation, and in situ thrombotic occlusion.
brain tissue that surrounds the core region of ischemia is
termed penumbra (surrounds the core region of non-
viable tissue) and can only be tolerated for a finite period Hemorrhagic Transformation
before permanent cellular injury and death ensue. Conversion of an ischemic infarction into a hemorrha-
At the onset of large-vessel ischemic stroke, such gic one, called hemorrhagic conversion, is due to the
as occlusion of the middle cerebral artery, there is a breakdown of the blood–brain barrier (BBB) with
region of core ischemia that becomes infarcted rapidly leakage of intravascular blood and its contents into
within minutes, as well as an area called the penumbra, injured ischemic or infarcted brain tissue or infarcted
which is potentially salvageable and amenable to throm- tissue. Subsequent continued bleeding can expand the
bolysis (e.g., issue plasminogen activator [tPA]) and hemorrhage similar to a primary intraparenchymal
reperfusion strategies. The most common complication hemorrhage. Careful control of blood pressure after
after infarction is the damage to the underlying paren- acute stroke within stated guidelines3 (< 180 mm Hg
chyma and the functional activity that area of the brain systolic after thrombolysis within the first 24 hours,
controlled. < 210 systolic without thrombolysis, or less than 160
after intracranial hemorrhage) is a primary means to
limit this complication as well as the avoidance of
Secondary Pathophysiologic Mechanisms unnecessary anticoagulants.
After the initial ischemic area evolves, secondary path-
ophysiologic mechanisms may occur that result in
further deterioration of neurologic status. These in- Mass Effect and Raised Intracranial Pressure
clude progression of the oligemic penumbra to infarc- Mass effect with subsequent raised ICP is another form
tion, hemorrhagic conversion of the ischemic infarct, of secondary brain injury (Fig. 2) that can result in
and the development of cerebral edema resulting in worsening of cerebral blood flow. One form of ischemic
increased intracranial pressure. In addition, recurrent stroke known to cause edema and significant mass effect
stroke and the development of seizures affect morbidity is that of the so-called malignant cerebral infarction.
and mortality. This typically occurs in the setting of an occlusion of the
internal carotid artery or the middle cerebral artery. In
such cases, massive cerebral edema can occur, causing
Progression of Penumbra to Infarction herniation3 and subsequent brain death.
Secondary brain injury and mechanisms are also impor- For patients with suspected raised ICP, place-
tant and a common cause of subsequent neurologic ment of an ICP monitor or ventriculostomy is required
deterioration after initial stroke. For example, a patient for aggressive therapy. An osmotic agent, such as

Table 1 Ischemic Stroke Complications

Cerebral Complications
Primary brain injury
Initial stroke: Neurologic and functional deficits, delirium
Recurrent stroke (9%)
Secondary brain injury
Stroke progression
Penumbra progression to infarction
Hemorrhagic conversion of ischemic infarct
Cerebral edema, mass effect, herniation, raised intracranial pressure
Hydrocephalus (communicating or noncommunicating)
Seizures 3%2 (higher in embolic strokes)
Stroke-specific complications
Neurologic breathing patterns (e.g., Cheyne-Stokes, cluster, apneustic, ataxic)
Autonomic dysfunction—acute hypertension, Cushing reflex
Depression/anxiety (12–16%2)
Pressure palsies (mononeuropathies) and critical illness myoneuropathy

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Pain—immobility, contractures, spasticity, or central pain syndrome
Extracerebral Complications
Head and neck
Angioedema after rtPA and/or ACEI/ARB38,39
Aspiration without pneumonia, aspiration pneumonia (24%2), pneumonitis,
Acute lung injury, pulmonary edema (e.g., cardiac or neurogenic),
ARDS, pulmonary embolism
Sodium and water homeostasis disturbance (e.g., SIADH)
Neurocardiogenic injury (e.g., Tako Tsubo cardiomyopathy, troponin ‘leak’)
Myocardial infarction, cardiogenic shock, pulmonary edema
ECG changes: arrhythmias, ST and T wave changes on ECG, atrial fibrillation
Cushing ulcer, gastrointestinal bleeding, ileus, malnutrition
Urinary tract infection (24%2)
Deep vein thrombosis (2–3%2)
Contractures and adhesive capsulitis
Decubitus ulcers (21%2), infections
Adapted from Langhorne P., et al. Stroke 2000;31:1223–1229.2
ACEI, ACE inhibitor; ARB, angiotensin receptor blocking agent; ARDS, acute respiratory distress syndrome; ECG, electrocardiogram; rtPA,
recombinant tissue plasminogen activator; SIADH, syndrome of inappropriate antidiuretic hormone hypersecretion.

mannitol or hypertonic saline, can be given to reduce patients with ischemic stroke, the CPP should be kept in
ICP,3,18 but often is a temporizing measure. For patients the range of 65 to 70 mm Hg or higher. Cerebral
with symptomatic mass effect, consideration may be perfusion pressure values greater than 130 may lead to
given to hemicraniectomy.3,18 Medical and surgical hyperemia, worsened cerebral edema, or hemorrhage.
management of malignant cerebral edema and the role
of hemicraniectomy in acute cerebral infarction is be-
yond the scope of this review.3,18 It is, however, impor- Recurrent Stroke
tant to remember that to prevent further ischemia, one Recurrent stroke occurs in 9% of patients after an
must maintain CPP. Cerebral perfusion pressure can be initial stroke within the first few weeks.2 (Fig. 1)
calculated once ICP and MAP are obtained from mon- Identification of the underlying stroke mechanism
itoring via the equation, CPP ¼ MAP – ICP. For most and targeting treatment remains the best way to reduce

Table 2 ‘‘ABC’s’’ of Stroke Management (American an embolic event with transient ischemia and subsequent
Heart Association Guidelines)3,18 reperfusion. Seizure, importantly, is no longer an abso-
A–Airway/aspiration, cardiac monitor  24 hour all patients, O2 lute exclusion for tPA.3 Approximately 1 to 2% of stroke
for hypoxic patients, intubation/mechanical ventilation for patients present with status epilepticus.24 Seizures cause
compromised airway—Class I secondary neurologic deterioration after stroke by in-
B–Blood pressure control specific to stroke type—Class II. creasing brain metabolic activity in vulnerable ischemic
Hypotension etiology should be evaluated and treated—Class I brain tissue. Burneo et al found that patients with
C–CPP (measure and control ICP if elevated)—Class II seizures had a higher mortality at 30 days (36.2% vs
D–DVT prevention with compression devices—Class I, if no 16.8%, p < 0.0001), at 1-year poststroke (48.6% vs
active bleeding risk, then consider SQ UFH or LMWH-Class II 27.7%, p < 0.001), had a longer hospitalization, and
E–Early mobilization—Class I greater disability at discharge (p < 0.001).23 Risk factors
F–Fever worked up & treated aggressively—Class I for seizure after stroke by multivariate analysis included
G–Glucose > 140 – 185 mg/dL, use insulin; hypoglycemia stroke severity, hemorrhagic stroke subtype, and the
should be treated—Class I presence of neglect on neurologic exam. The authors
CPP, cerebral perfusion pressure; DVT, deep vein thrombosis; ICP,
concluded that seizures after stroke increased resources
intracranial pressure; LMWH, low-molecular-weight heparin; SQ, utilization, hospital length of stay, and increased both
subcutaneous; UFH, unfractionated heparin. 30-day and one-year mortality. Recurrent seizures de-
velop in 2% to 33% of poststroke patients, particularly of

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subsequent stroke risk (e.g., atrial fibrillation, and the embolic stroke type.3 Late seizures vary in incidence
eventual anticoagulation). from 3% to 67%, and appear higher in patients with
preexisting dementia.3 Treatment of seizure with anti-
epileptic agents is individualized to the patient and
Seizures recommended.3
Seizures are common after stroke, occurring in 3% of
patients,18,23 particularly within the first 24 hours after
stroke, and are typically partial with or without secon- EXTRACEREBRAL (SYSTEMIC)
dary generalization. A seizure may herald the onset of a COMPLICATIONS
stroke due to reduced seizure threshold from cortical
excitation and ischemia. A seizure may also occur from Aspiration Pneumonia and Pneumonitis
Aspiration is common after stroke due to impaired
swallowing and protective reflexes that fail to prevent
material entering the trachea and lower airways. Aspira-
tion can be due to depressed level of consciousness with
frank (or silent) aspiration of gastrointestinal contents,
or may be due to dysphagia or impaired swallowing
function. Impaired swallowing and impairment of other
brainstem reflexes may lead to aspiration of normal
airway secretions that are typically swallowed on an
unconscious level. Such aspiration of gastrointestinal
contents or upper airway contents can lead to aspiration
pneumonia or pneumonitis.
One of the most crucial factors in preventing
aspiration pneumonia is screening for dysphagia at
stroke presentation. A patient failing a bedside screening
test25 should be made NPO (nothing by mouth) until a
suitable means of nutrition or liquid can be given to the
patient in a safe manner. Until that time, the patient can
be given intravenous (IV) fluids. Temporary placement
of nasogastric tubes can be considered. If the patient
cannot safely swallow material or maintain nutritional
goals by oral diet by hospital discharge, a percutaneous
Figure 2 Mass effect and downward displacement of the gastrostomy tube is often considered.
brainstem (herniation). Herniation not only displaces brain Another strategy to prevent aspiration is intubat-
tissue, but also causes vascular injury to brain tissue by ing patients who are comatose and not protecting their
compressing perforating arteries and arterioles. (Permission airway.3 This may reduce, but not completely eliminate,
Mayo Foundation for Medical Education. All rights reserved). aspiration risk. If there is clinical suspicion of aspiration,

tPA) has been given.3 If a thrombolytic agent is admin-

istered, the blood pressure should be treated if greater
than 185/110 mm Hg. Severe uncontrolled hypertension
with a MAP higher than 130 or 150 mm Hg is felt to
increase the risk of intracranial hemorrhage after throm-
bolysis. The exact target of blood pressure has yet to be
established; however, a reasonable goal is lowering the
blood pressure by 15% to 25% if the blood pressure is
elevated over the first 24 hours.3 Short-acting antihy-
pertensive agents (e.g., labetalol, hydralazine) are typi-
cally used to prevent overshooting the target.3
Hypotension (e.g., systolic < 110 mm Hg or
MAP <70 in nonhypertensive patients or 10 mm Hg
or more points below a chronic hypertensive patient’s
baseline MAP in the setting of ischemic stroke is known
to be harmful.3 Acute hypotension should be immedi-
ately treated (e.g., fluid bolus if dehydrated or volume
depleted, or occasionally vasopressor agents) and causes

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of the hypotension investigated (e.g., myocardial infarc-
tion or injury, sepsis/bacteremia, vasovagal response,
Figure 3 Chest radiograph shows aspiration pneumonia in
the right lower lobe.
Venous Thromboembolism (VTE)
Deep vein thrombosis (DVT) (Fig. 4) is a common
further evaluation is required. It is important to eval- complication after stroke due to limb paresis and im-
uate patients that may have aspirated at the time of the mobility. Asymptomatic DVT has been reported in 18%
stroke or subsequently by chest auscultation as well as a to 40% of stroke patients, typically in the affected paretic
chest radiograph. If there is evidence of an infiltrate limb.3,18 Clinically symptomatic DVT (limb pain, swel-
(Fig. 3), antibiotic treatment is recommended.3 Pa- ling, and/or fever) may occur in 3% to 5% of stroke
tients who aspirate, but do not develop a frank infiltrate patients.26–31 Deep vein thrombosis risk factors include
on chest radiograph, may still develop a transient advancing age, paretic limb/immobility, dehydration,
productive cough, a low-grade fever, and a self-limited and most importantly, stroke severity (i.e., NIH Stroke
pneumonitis. In such patients, a full course of anti- Scale).3,26–28 Deep vein thrombosis may develop within
biotics may not be warranted (e.g., risks of C. difficile 1 week of immobility, and the risk of DVT often persists
colitis from antibiotics may outweigh the benefit). in patients in nursing homes after acute hospitaliza-
However, stroke patients with cough and fever should tion.26
be observed closely for the development of pneumonia Pulmonary embolism (PE) is the most feared
clinically or on a subsequent chest radiograph. Anti- complication in patients harboring a DVT. Half of
biotics are recommended once an infiltrate or pneumo- patients with symptomatic PE die at presentation, thus
nia is detected. Patients with massive aspiration may stressing the importance of prevention.
develop acute lung injury or acute adult respiratory Aspirin alone is insufficient for DVT–PE pre-
distress syndrome (ARDS) and require intubation and vention,31 but provides a small benefit for secondary
mechanical ventilation, bronchoscopy, and bronchoal- ischemic stroke prevention.32 Several studies evaluated
veolar lavage. the role of unfractionated heparin (UFH) in venous
thromboembolism (VTE) prevention. The IST
Trial33,34 was the largest UFH trial performed to date
Acute Hypertensive Response with 19,435 stroke patients. The study allocated half of
Blood pressure management is important in patients the patients to unfractionated heparin (5000 or 12,500
with acute ischemic or hemorrhagic stroke. Patients IU subcutaneously BID twice daily) and half did not
with chronic hypertension may require relatively higher receive heparin. In a factorial design, half of the patients
levels of MAP from both a systemic and brain perfusion were also allocated to aspirin 300 mg daily and half to no
standpoint. Current guidelines recommend that emer- aspirin. Thus, 6 different treatment allocations were
gent antihypertensives should be withheld in patients possible. The primary endpoint was death by 14 days,
with acute ischemic stroke unless the blood pressure and secondary death or dependency at 6 months. The
exceeds 220/100 mm Hg or a thrombolytic agent (e.g., rate of pulmonary embolism in those allocated to heparin

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Figure 4 Upper image: Deep vein thrombosis (DVT) with pulmonary embolism. Lower left: Sequential compressive device.
Lower right: Vena cava filters. (Permission Mayo Foundation for Medical Education. All rights reserved).

was 0.5% compared with 0.8% in those not allocated to confirmed a role for heparin in prevention of VTE.
receive heparin. There was no significant difference in Treatment with LMWH was associated with significant
the rate of PE in those allocated to aspirin versus those reductions in DVT and PE; however, there was an
that did not receive it. The rate of major hemorrhage increase in major extracranial hemorrhage. The studies
in the heparin group was 1.3% compared with 0.4% in included in this meta-analysis, however, were designed
those not receiving heparin. mainly around the primary endpoint of stroke outcome
A meta-analysis of studies evaluating low-molec- and reduction of recurrent stroke. Thus, VTE was a
ular-weight heparin (LMWH) in acute ischemic stroke secondary endpoint.

The PREVAIL (Prevention of Venous Although the study reported a reduction in DVT in the
Thromboembolism after Acute Ischemic Stroke) Trial28 stockings group, the reduction was not significant.30
was the largest trial comparing LMWH enoxaparin Pneumatic sequential compression devices (SCDs)
40 mg subcutaneously daily against UFH 5000 IU every are best studied in postoperative patients and less well
12 hours in 1,762 nonambulatory ischemic stroke pa- studied in patients with stroke.31 SCDs can be used in
tients. The rates of symptomatic DVT between the combination with UFH or LMWH for high-risk DVT
LMWH group and the UFH group were not signifi- patients; however, there is no evidence to suggest added
cantly different (p ¼ 0.18). However, the rates of asymp- benefit or harm. These devices used alone are best
tomatic DVT detected by ultrasound were statistically reserved for patients who cannot receive anticoagulants.
less prevalent in the low-molecular-heparin group versus Some patients may require an inferior vena cava
the unfractionated heparin group (p < 0.0001). The rate (IVC) filter (Fig. 4). According to the American Heart
of symptomatic ICH in each group was 1% (n ¼ 4 Association guidelines,3,18 ischemic stroke patients who
occurred on enoxaparin, 3 of whom died) compared cannot receive anticoagulants and have a confirmed
with n ¼ 6 on UFH, 4 of whom died, which was not DVT should be considered for an IVC filter. It is
statistically significant. Higher initial NIH Stroke Scale important to note that little data exists regarding the
(e.g., > 14) predicted bleeding. Symptomatic extracra- long-term safety of IVC filters, the ability for the filter to
nial bleeding was 1% in enoxaparin group (2 fatal) and prevent small emboli, and the length of time the filter
0% in UFH. should be left in place.3 Complications from IVC filters

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Several unresolved questions remain regarding include partial or even complete occlusion of the IVC
venous thromboembolism prophylaxis in patients with filter leading to IVC obstruction.
ischemic stroke. The optimum duration of VTE pro-
phylaxis remains unanswered as clinical trials are often
limited to less than 2 weeks, but risk often persists Cardiac Complications after Stroke
beyond this period. It is also unclear if there is a superior Cardiac complications and electrocardiogram (ECG)
agent and at what dose: fixed dose versus weight based changes are common after stroke. One type of compli-
LMWH, UFH 5000 twice daily, or UFH 5000 3 times cation is neurocardiogenic injury. Neurocardiogenic in-
daily. In a Cochrane analysis by Sandercock et al com- jury is defined as cardiac injury that results from a
paring ischemic stroke patients treated with either enox- primary neurologic insult such as a stroke. Neurocardio-
aparin 40 mg daily or unfractionated heparin 5000 IU genic injury can cause ECG changes and even troponin
TID, the rate of DVT PE was 19.7% in the enoxaparin elevation. Pathologically this type of injury is felt to be
group compared with 33.4% in the UFH group.27 related to contraction band necrosis rather than coagu-
However, the rates of symptomatic DVT PE and intra- lation necrosis seen in coronary occlusion and myocardial
cranial hemorrhage were not significantly different.27 At infarction (MI). Initially, it can be difficult to discrim-
present, consensus guidelines3 recommend either UFH inate between a stress-induced neurocardiogenic injury
or LMWH for nonambulatory patients with stroke. from a true acute myocardial infarction (AMI) from
Although commonly used, data do not show underlying coronary artery disease. However, neurocar-
efficacy for reducing VTE with the use of thigh high diogenic injury, especially when severe, typically has a
hose. The CLOTS 1 trial investigated this in 2,518 ‘‘left ventricular apical balloon pattern.’’ This is also
acute stroke (ischemic or hemorrhagic) patients.29 The known as Tako Tsubo (named after the shape of an
patients were randomized to routine care plus leg stock- ‘‘octopus pot’’ due to its characteristic ventriculogram
ings or routine care plus avoidance of stockings. Patients and echocardiogram appearance), which has an anterior
were assessed by Doppler ultrasound of the legs at 7 to and apical wall akinesis or hypokinesis. This is in con-
10 days and again between 25 and 30 days. The primary trast to a coronary distribution MI, which typically has
endpoint was symptomatic or asymptomatic DVT in the an ECG and echocardiogram appearance of dysfunction
popliteal or femoral veins. The results showed a 10% rate in the vascular territory of the coronary vessel. The right
of DVT in patients with stockings compared with 10.5% coronary artery distribution usually affects the right
without the stockings, which was a nonsignificant re- lateral ventricle wall and base, whereas the left anterior
duction in risk. The patients with stockings were more descending artery distribution is the anterior two-thirds
likely to have skin breaks, ulcers, blisters, and skin of the heart. Tako Tsubo cardiomyopathy after stroke
necrosis than did patients without the stockings. The also typically improves in terms of the ejection fraction
data do not support the use of stockings for DVT on echocardiogram within a few weeks time compared
prevention in stroke patients. Further, a small study with a frank MI, which may leave permanently reduced
investigated the use of compression stockings in 97 left ventricular ejection fraction. Serial troponins and
immobile patients admitted to an acute stroke unit, 65 ECGs, as well as an echocardiogram and cardiology
of whom were allocated to receive stockings and 32 of evaluation, are useful in helping to distinguish between
whom were allocated to usual care without stockings. these two entities and to help with management.

Figure 5 Stages of decubitus ulcers.

Stroke and coronary artery disease (CAD) are also stroke severity, female sex, and use of urinary catheters.3
comorbidities.35,36 Stroke risk is highest within 3 months Bacteriuria is common in catheterized patients; thus, a
of a MI.35,36 One third of stroke patients have CAD (or diagnosis of UTI in catheterized patients requires a
silent CAD).35,36 Three percent of stroke patients die culture in addition to the urinalysis. Prevention is key
from cardiac event in less than 90 days. In addition, in stroke patients. Overuse of catheters is common. This
stroke may be the presenting sign of an MI in a small can be simply overcome by reviewing the daily need for a
percentage of patients (ventricular dysfunction). To urinary catheter, as well as other invasive lines, and

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further complicate this issue, aphasic patients may not discontinuing them at the first available opportunity.
complain of chest pain or may be diaphoretic and Recent guidelines do not recommend prophylactic anti-
tachycardic, which is nonspecific. Management of biotics to prevent urinary infection.3 Acidification of
MI after stroke typically includes starting or continuing urine with ascorbic acid may be helpful, in addition to
aspirin (if permitted from cerebrovascular standpoint) as treating urinary tract infection with antibiotics when
soon as possible. For patients who received tPA, aspirin present.
is withheld for 24 hours after tPA, then can be restarted
assuming there is no significant intracranial hemorrhage.
Supplemental oxygen and morphine are typically admin- Decubitus Ulcers
istered for MI, the latter agent for chest pain or angina to Decubitus ulcers (Fig. 5) are an underrecognized prob-
reduce myocardial oxygen consumption. Intravenous lem in hospitalized patients with stroke. Decubitus
nitroglycerin or sublingual nitrates should be given if ulcers can lead to progressive skin erosion and potentially
blood pressure is elevated, but with caution in acute even osteomyelitis. Risk factors for a decubitus ulcer
stroke patients as these may cause hypotension, which include immobility, poor nutrition, lack of turning,
can make the stroke worse. Consultation with a cardiol- urinary incontinence, and lack of wound care or proper
ogist is advised when there is a concern for active nursing. Strategies to minimize decubitus ulcer forma-
coronary ischemia and to help define an optimal blood tion include daily nursing documentation about the
pressure and heart rate. For tachycardic patients, heart patient’s skin status, early recognition, and intervention
rate control with b-blockers (IV metoprolol) can be including bed turns every 2 hours, barrier creams and
used, albeit cautiously to control rate with less effect cleaning, early mobilization by physical therapy, and
on blood pressure. If anemia is present (e.g., hematocrit optimizing nutrition. When a decubitus ulcer is present,
less than 30%), blood transfusion may reduce early consulting a wound care specialty nurse or implementing
mortality in elderly patients with acute myocardial in- the use of specialized mattresses can be helpful. For stage
farction.37 Finally, statin medications and subcutaneous IV wounds, a wound ‘‘VAC’’ and a consultation with a
or IV heparin have been shown to reduce mortality after plastic surgeon for a graft may be helpful. Hospital-
MI, and may be used if safe from the cerebrovascular acquired decubitus ulcers are considered a quality metric
standpoint. for many hospitals. In addition, the Center for Medicare
Services (CMS) does not reimburse wound care if the
patient develops decubiti while hospitalized due to the
Urinary Tract Infections potentially preventable nature of this complication.
Urinary tract infections (UTIs) occur frequently in
patients with stroke. Patients with stroke may be limited
in describing symptoms, such as urinary frequency or SPECIAL CONSIDERATION—
pain with urination, due to stroke-related disability ANGIOEDEMA AFTER TISSUE
(aphasia, dysarthria, level of consciousness) or because PLASMINOGEN ACTIVATOR
they have an indwelling catheter. Often, fever in iso- Angioedema that forms after the use of IV-tPA can
lation is the manifestation that alerts clinicians to search cause life-threatening airway obstruction and respiratory
for a UTI. Risk factors for UTI include advancing age, and cardiopulmonary arrest.38,39 The main risk factors

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15. Ellekjaer H, Holmen J, Indredavik B, Terent A. Epidemi-
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