Complications of Stroke - An Overview - UpToDate

19/9/2019 Complications of stroke: An overview - UpToDate
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Complications of stroke: An overview

Author: Koto Ishida, MD
Section Editor: Scott E Kasner, MD
Deputy Editor: John F Dashe, MD, PhD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2019. | This topic last updated: Aug 21, 2019.
INTRODUCTION
Complications of acute stroke are common. They increase the risk of poor clinical outcomes.
Preventative strategies and treatments are available and should be used when appropriate.
MEDICAL COMPLICATIONS
The rates of reported medical complications of stroke are high (table 1 and table 2) [1-5]. Serious
complications include pneumonia, urinary tract infection, gastrointestinal bleeding, myocardial
infarction, deep vein thrombosis, and pulmonary embolism.
Incidence rates vary across studies, but improving care may be reducing complication rates. In
one prospective longitudinal study, the frequency of one or more medical complications within the
first week after stroke declined from 2003 to 2013 by 36 percent [6].
The presence of any in-hospital medical complication, many of which are preventable, has been
associated with a significantly increased risk for 30-day readmission (adjusted hazard ratio 1.68;
95% CI 1.04-2.73) [7].
Dysphagia — Dysphagia is a common complication of stroke and is a major risk factor for
developing aspiration pneumonia. Dysphagia related to stroke is more precisely characterized as
oropharyngeal dysphagia, defined by swallowing impairment of the upper digestive tract. This
definition has been extended to capture impairments in swallowing efficiency and safety, including
delays in the timing of movements, reduced range of movements, and frank aspiration [8].
Aspiration in this population is usually a sign of severe dysphagia, and refers to abnormal entry of
fluid, particulate exogenous substances, or endogenous secretions into the airways.
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These observations are supported by a systematic review of 24 studies that evaluated

oropharyngeal dysphagia and aspiration in adult patients with stroke [8]. In pooled analysis of
studies with sufficient data, the risk of pneumonia was increased with dysphagia compared with no
dysphagia (relative risk [RR] 3.17, 95% CI 2.07-4.87) and especially with aspiration compared with
no aspiration (RR 11.56, 95% CI 3.36-39.77).
The incidence of dysphagia after stroke was lowest when identified by screening methods, mainly
water swallow (37 to 45 percent) [8]. The incidence was intermediate when identified by a trained
swallowing clinician (51 to 55 percent), and it was highest when identified by instrumental testing,
mainly videofluoroscopy (64 to 78 percent). The dysphagia rates may have been overestimated by
instrumental testing, which can reveal movement patterns that reflect the normal effects of aging;
these were not distinguished from pathologic dysphagia by the definitions used in the studies.
Independent predictors of dysphagia on initial presentation include male gender, age greater than
70, disabling stroke, impaired pharyngeal response, incomplete oral clearance, and palatal
weakness or asymmetry [9]. Dysphagia usually improves spontaneously with return of safe
swallowing function by two weeks in approximately 90 percent of patients [8,10,11]. However, a
significant minority of patients have persistent dysphagia.
● Screening for dysphagia – We evaluate swallowing function using a water swallow test at
the time of admission for all patients with acute stroke before administering oral medications
or food. The water swallow test is simple and quick to perform. Videofluoroscopy with
modified barium swallow can be performed once the patient is stable in order to assess the
severity of oropharyngeal dysfunction and risk of aspiration. (See "Oropharyngeal dysphagia:
Clinical features, diagnosis, and management", section on 'Videofluoroscopic modified barium
swallow'.)
In a prospective, multicenter study, use of a formal screening protocol for dysphagia (eg,
water swallow test) for all patients admitted with stroke was associated with a significantly
decreased risk of aspiration pneumonia compared with no formal screen (adjusted odds ratio
0.10, 95% CI 0.03-0.45) [12]. The pneumonia rates at sites with and without a formal
dysphagia screen were 2.4 versus 5.4 percent, for an absolute risk reduction of 3 percent.
Bedside tests to screen for swallowing dysfunction are useful but have a lower sensitivity
compared with more comprehensive testing [13-16]. In a 2016 systematic review and meta-
analysis of 11 studies and 770 patients with stroke, the water swallow test for aspiration had a
sensitivity of 64 to 79 percent and a specificity of 61 to 81 percent [15]. One study found that
the best bedside predictors of aspiration to thin liquid were spontaneous cough during test
swallows and the overall sense of the presence of aspiration by the examiner [17]. A 2012
systematic review found that cough or voice change in response to bedside water swallow
test had a low to moderate sensitivity and moderate to high specificity for predicting aspiration
[18].

● Preventing aspiration – Prevention of aspiration for patients with acute stroke includes initial
nil per os (NPO) status for those who may be at risk for aspiration and subsequent dietary
modifications for those who have persistent dysphagia. Intravenous hydration with normal
saline should be administered to maintain volume status [19]. (See "Oropharyngeal
dysphagia: Clinical features, diagnosis, and management".)
Patients with acute stroke who cannot take food and fluids orally due to persistent dysphagia,
altered mental status, and/or mechanical ventilation should receive nutrition and hydration via
nasogastric, nasoduodenal, or percutaneous endoscopic gastrostomy tube feedings while
undergoing efforts to restore swallowing [14,20]. In most cases, a nasogastric tube should be
placed within 48 hours of stroke onset if enteral nutrition is likely to be needed for less than
four weeks; nasogastric tube placement may be placed sooner if necessary to administer oral
medications.
Ideally, percutaneous gastrostomy tube placement can be deferred for two to four weeks to
determine whether spontaneous recovery of swallowing will develop and to allow time to
discuss the risks and benefits of gastrostomy tube insertion. However, observational data
from the United States suggest that the median time to placement is closer to seven days for
patients with stroke [21]. Early gastrostomy tube placement is probably driven in part by
requirements for disposition, since nasogastric tube feeding is not an option at many acute
rehabilitation facilities. (See "Nutrition support in critically ill patients: An overview" and
"Gastrostomy tubes: Uses, patient selection, and efficacy in adults" and "Enteral feeding:
Gastric versus post-pyloric".)
Venous thromboembolism — Venous thromboembolism (VTE) encompasses deep vein

thrombosis (DVT) and pulmonary embolism, which is potentially life-threatening. VTE prophylaxis
is indicated for all patients with acute stroke who have restricted mobility. The approach to
prevention and treatment of VTE is reviewed in detail separately. (See "Prevention and treatment
of venous thromboembolism in patients with acute stroke".)
Infection
Pneumonia — Pneumonia develops in 4 to 10 percent of patients with acute stroke

[2,4,6,22,23]. Stroke-related pneumonia is associated with a higher mortality and a poorer long-
term outcome [4,22,24].
● Risk factors and causes – Risk factors for in-hospital pneumonia include older age,
dysarthria, dysphagia, aphasia, stroke severity, cognitive impairment, use of gastric acid
suppressive medications, and an abnormal water swallow test [25-28].
Aspiration is the cause of about 60 percent of post-stroke pneumonia [2]. Aspiration

pneumonia refers to the pulmonary consequences resulting from the abnormal entry of fluid,
particulate exogenous substances, or endogenous secretions into the lower airways. Most
pneumonia arises following the "aspiration" of microorganisms from the oral cavity or
nasopharynx. Aspiration pneumonia following stroke is usually due to stroke-related
dysphagia (ie, impairment of motor and sensory mechanisms involved in deglutition) or to a
decreased level of consciousness that results in compromise of the cough reflex and glottic
closure. (See 'Dysphagia' above.)
● Prevention — Measures to prevent aspiration pneumonia in patients with dysphagia include

initial nil per os (NPO; nothing by mouth) status and subsequent dietary modifications for
those who have persistent dysphagia. (See "Oropharyngeal dysphagia: Clinical features,
diagnosis, and management".)
Screening on admission for swallowing difficulty is an important measure to prevent

pneumonia in patients with acute stroke, as discussed above. (See 'Dysphagia' above.)
Additional preventive measures include patient mobilization when neurologically stable and
good pulmonary care [19]. For intubated patients, risk reduction measures include daily
assessment for potential extubation, minimizing sedation, suctioning of secretions, elevating
the head of the bed when possible, and maintaining ventilator circuits. (See "Risk factors and
prevention of hospital-acquired and ventilator-associated pneumonia in adults".)
Given the apparent increased risk of hospital-acquired pneumonia associated with the use of
histamine-2 receptor antagonists and proton pump inhibitors, we avoid agents that suppress
gastric acid in patients who are not at high risk of developing a stress ulcer or stress gastritis.
Prophylactic antibiotics for patients with acute stroke do not reduce the incidence of
poststroke pneumonia or improve functional outcomes [29,30]. A number of other
interventions (eg, positioning, drugs, oral hygiene, tube feeding, influenza vaccination,
pneumococcal vaccination) have been proposed to prevent aspiration in hospitalized and
nonhospitalized older adult patients. However, no clinical trials have evaluated the utility of
these measures specifically in patients with stroke. (See "Aspiration pneumonia in adults" and
"Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in
adults" and "Pneumococcal vaccination in adults" and "Seasonal influenza vaccination in
adults".)
● Diagnosis and management – The diagnosis and management of hospital acquired

pneumonia is reviewed elsewhere. (See "Treatment of hospital-acquired and ventilator-
associated pneumonia in adults".)
Urinary tract infection — Urinary tract infection occurs in 11 to 15 percent of patients followed
for up to three months after acute stroke [1,4] and constitutes a serious complication (ie,
prolonged, immediately life threatening, or resulting in hospitalization or death) in about 1 percent
[2]. Urinary tract infection remains a common complication when patients are followed for up to 30
months [1].

● Risk factors and causes – In a meta-analysis, the main risk factors for urinary tract infection
were female sex, older age, higher modified Rankin Scale score (a measures of poststroke
disability), and postvoid residual volume >100mL [31].
It is common practice to place indwelling bladder catheters in patients with stroke due to
immobility, incontinence, urinary retention, or convenience. However, placement of an
indwelling bladder catheter is an important risk factor for infection, and the duration of
catheterization is directly related to risk of urinary tract infection [32].
● Prevention – The use of indwelling urinary catheters should be avoided whenever possible
[14]. The use of external catheter systems (ie, condom catheters for men, adhesive urinary
pouches for women) or intermittent catheterizations are alternatives that may be associated
with a lower risk of urinary tract infections compared with an indwelling urethral catheter.
However, supporting data are scant. (See "Placement and management of urinary bladder
catheters in adults" and "Complications of urinary bladder catheters and preventive
strategies" and "Catheter-associated urinary tract infection in adults".)
● Diagnosis and management – We screen for urinary tract infection if patients have signs of
infection (eg, fever, leukocytosis), unexplained altered mental status, or suggestive
symptoms. Classic manifestations of urinary tract infection include dysuria, urinary frequency
or urgency, suprapubic pain, or flank pain, often accompanied by fever, chills, and/or elevated
peripheral white blood cell count. Urine cultures are important in diagnosing catheter-related
urinary tract infection. The vast majority of patients with symptomatic bacteriuria (ie, urinary
tract infection) have bacterial culture growth ≥105 colony forming units (CFU)/mL or fungal
growth in urine. (See "Catheter-associated urinary tract infection in adults", section on 'Clinical
features'.)
Most patients with catheter-related urinary tract infection are asymptomatic and do not have
elevated peripheral white counts. Treatment of asymptomatic bacteriuria does not improve
patient outcomes and increases the likelihood of emergence of resistant bacteria. Thus, with
few exceptions, screening and treatment for asymptomatic bacteriuria in catheterized patients
is not indicated. (See "Catheter-associated urinary tract infection in adults", section on
'Asymptomatic bacteriuria'.)
After the diagnosis is made, treatment options should be tailored to the culture results and
regional organism sensitivities. Bladder catheter management, methods to reduce the risk of
infection associated with indwelling catheters, and treatment of catheter-associated urinary
tract infection are reviewed elsewhere. (See "Catheter-associated urinary tract infection in
adults".)
Issues related to acute cystitis, recurrent urinary tract infection, and acute pyelonephritis are
discussed separately. (See "Acute simple cystitis in women" and "Acute simple cystitis in

men" and "Recurrent simple cystitis in women" and "Acute complicated urinary tract infection
(including pyelonephritis) in adults".)
Cardiac complications — Myocardial infarction, cardiac arrhythmias, and neurogenic cardiac

injury are potential complications of acute stroke.
Myocardial infarction — All patients with acute stroke should have electrocardiography (ECG)
and troponin level on admission, and continuous cardiac monitoring at least the first 24 hours of
admission [14,33]. Data from the modern era suggest that myocardial infarction (MI) occurs in
approximately 1 to 2 percent of patients with acute stroke during initial hospitalization and is
associated with poor outcome [2,6,34].
MI should be suspected for patients who have chest pain, shortness of breath, new heart failure,
or sudden cardiac arrest. The diagnosis of MI is supported by the presence of ST and/or T wave
changes on ECG, positive cardiac biomarkers, or hemodynamic abnormalities. (See "Diagnosis of
acute myocardial infarction".)
● Elevated cardiac enzymes – Cardiac troponin is the standard blood-based test to confirm
the diagnosis of acute myocardial infarction (see "Diagnosis of acute myocardial infarction",
section on 'Definitions'). However, troponin is not specific for acute thrombotic occlusion of a
coronary artery, the most common precursor to acute myocardial infarction. Increased blood
concentrations of cardiac troponin can also be seen in a variety of other diseases (table 3),
including acute stroke. In such cases, elevation of troponin and other cardiac enzymes after
acute stroke may be related to stroke-induced autonomic dysfunction or other types of
nonischemic myocardial injury. (See "Elevated cardiac troponin concentration in the absence
of an acute coronary syndrome", section on 'Acute stroke'.)
Limited retrospective data suggest that elevated troponin on admission for acute stroke is
associated with embolic stroke of unknown source (ESUS) and cardioembolic stroke [35], but
further studies are needed to confirm this finding.
● ECG abnormalities – The ECG is an essential diagnostic test for patients with possible or
established myocardial ischemia, injury, or infarction (see "Electrocardiogram in the diagnosis
of myocardial ischemia and infarction"). Abnormalities are manifest in the ST-segment, T
wave, and QRS complex. However, the ECG may be normal or nonspecific in a patient with
either myocardial ischemia or MI. Furthermore, ECG abnormalities that appear to represent
myocardial ischemia or infarction may be present for other reasons. ECG changes may occur
in the setting of stroke, likely mediated by the autonomic nervous system, particularly related
to subarachnoid hemorrhage. These include QT prolongation, T wave abnormalities, ST
segment elevation, and aberrant Q waves. These abnormalities may also represent
preexisting coronary disease [36].

● Management – The management of patients with suspected acute coronary syndrome (MI,
unstable angina) is reviewed separately. (See "Initial evaluation and management of
suspected acute coronary syndrome (myocardial infarction, unstable angina) in the
emergency department" and "Overview of the acute management of ST-elevation myocardial
infarction" and "Overview of the acute management of non-ST elevation acute coronary
syndromes".)
Arrhythmias — Cardiac arrhythmias are frequently present in the setting of acute stroke
[37,38], stressing the importance of continuous cardiac monitoring in the initial phase of stroke
management. In many cases, the cardiac rhythm disturbances likely were present prior to the
stroke and were not directly related to the stroke [39]. Symptomatic arrhythmias generally require
management in an intensive care unit setting with cardiology consultation.
In a prospective study of 501 patients with acute stroke, potentially serious cardiac arrhythmia
events occurred in 126 patients (25 percent) during the first 72 hours after admission to a
monitored stroke unit [37]. Tachycardia occurred mainly with atrial fibrillation; other causes
included focal atrial tachycardia, undetermined supraventricular tachycardia, ventricular ectopy,
nonsustained ventricular tachycardia, and atrial flutter. Bradyarrhythmias were caused by atrial
fibrillation, Mobitz type II atrioventricular block, asystole/sinoatrial block, and complete
atrioventricular block.
Neurogenic cardiac damage — A wide spectrum of regional left ventricular wall motion
abnormalities, typically but not always reversible, can occur with subarachnoid hemorrhage and
less often with other types of stroke [40]. Some patients develop a pattern of transient apical left
ventricular dysfunction that mimics myocardial infarction, but in the absence of significant coronary
artery disease [41]. This condition is known as takotsubo cardiomyopathy. (See "Aneurysmal
subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Clinical manifestations and
diagnosis of stress (takotsubo) cardiomyopathy".)
Stroke-induced cardiac damage is uncommon but is well-described [42,43]. It is unlikely that the
only mechanism explaining cardiac damage after acute stroke is the presence of underlying
coronary disease, particularly since signs of cardiac damage may occur in patients with
subarachnoid hemorrhage, who are often young and without underlying heart disease. In addition,
the rapid appearance and disappearance of the ST changes argue against macrovascular factors
and in favor of neural factors [44,45]. Myocardial injury in these cases is most likely the result of a
centrally mediated release of catecholamines caused by stroke-related brain injury. This type of
cardiac injury is similar to stress cardiomyopathy (also called takotsubo cardiomyopathy)
characterized by transient regional systolic dysfunction of the left ventricle (LV), mimicking
myocardial infarction, but in the absence of angiographic evidence of obstructive coronary artery
disease or acute plaque rupture. (See "Clinical manifestations and diagnosis of stress (takotsubo)
cardiomyopathy".)

Cardiac myofibrillar degeneration has been described in patients who die from acute stroke, and is
histologically identical to the cardiac lesions of catecholamine infusion, "voodoo death,"
hypothalamic stimulation, or reperfusion of transiently ischemic cardiac muscle [42]. The
myofibrillar degeneration occurs in the vicinity of the cardiac nerves, and not in the macrovascular
distribution seen in patients with coronary disease [42,46]. The lesion also differs from the
necrosis seen in coronary disease because it is visible within minutes of onset, and the cells die in
a hypercontracted state with contraction bands, associated mononuclear infiltration, and early
calcification.
Accumulating experimental and clinical evidence suggests that stroke involving the insular cortex
may be associated with adverse cardiac outcomes including repolarization abnormalities,
arrhythmias, neurogenic cardiac damage, heart failure, and sudden death [47-53]. The presumed
biologic basis for this association is the role of the insular cortex in the autonomic control of
cardiovascular function [48,52-60].
Pulmonary complications — Serious pulmonary complications of stroke include pneumonia,

neurogenic pulmonary edema, and the need for intubation and mechanical ventilation [61].
● Pneumonia – Pneumonia is a common cause of fever within the first 48 hours of acute
stroke. Aspiration is the most frequent cause of poststroke pneumonia, and it is usually due to
stroke-related dysphagia or to decreased level of consciousness. (See 'Pneumonia' above
and 'Dysphagia' above.)
● Need for mechanical ventilation – Intubation and mechanical ventilation of patients with
ischemic stroke is usually performed to treat pulmonary edema or for inability to protect the
airway. Additional indications include partial airway obstruction, hypoventilation, and
aspiration pneumonia. (See "Overview of mechanical ventilation" and "Physiologic and
pathophysiologic consequences of mechanical ventilation", section on 'Central nervous
system'.)
● Neurogenic pulmonary edema – Neurogenic pulmonary edema (NPE) is reviewed here

briefly and discussed in detail elsewhere. (See "Neurogenic pulmonary edema".)
Neurogenic pulmonary edema (NPE) is an increase in interstitial and alveolar fluid that occurs
in the setting of head trauma, seizures, or stroke, particularly subarachnoid hemorrhage (table
4). NPE most often develops abruptly and progresses quickly after the onset of the neurologic
insult. The typical patient with NPE is dyspneic, tachycardic, and hypertensive, with bilateral
rales. Most cases of NPE resolve spontaneously and are well tolerated, but the condition can
be fatal in severe cases. Treatment of NPE is largely supportive and directed mainly towards
treatment of the underlying neurologic condition.
● Abnormal respiratory patterns – Abnormal respiratory patterns may complicate stroke;

these include Cheyne-Stokes breathing, periodic breathing, apneustic breathing, central sleep
apnea, ataxic breathing, and failure of automatic breathing (figure 1). (See "Disorders of
ventilatory control".)
Sleep-related breathing disorders — The relationship of sleep-disordered breathing (including

both obstructive sleep apnea and central sleep apnea syndrome) as a possible risk factor for
stroke and as a possible complication of stroke is discussed separately. (See "Sleep-related
breathing disorders and stroke".)
Gastrointestinal bleeding — Gastrointestinal (GI) hemorrhage affects 1.5 to 3 percent of patients

with acute stroke [2,62,63]. Patients with acute stroke and GI hemorrhage have worse outcomes,
with higher rates of dependency and mortality. Overt GI bleeding may be severe or even life-
threatening and manifests with hematemesis, melena, or hematochezia. Occult GI bleeding (ie, no
visible evidence of bleeding) is generally less serious; it is suspected in the setting of iron
deficiency anemia or a positive fecal occult blood test.
● Risk factors – Retrospective data from various studies suggest that risk factors for GI
hemorrhage include older age, severe stroke, posterior circulation stroke, infection, history of
hypertension, hepatic cirrhosis, prestroke dependence, and a history of peptic ulcer disease
or cancer predating the incident stroke [62-65].
● Prevention – GI stress ulcer prophylaxis with proton pump inhibitors or H2 antagonists is

effective for reducing overt GI bleeding, but may increase the risk of nosocomial pneumonia.
Therefore, stress ulcer prophylaxis is not used routinely for patients with acute stroke, but is
reserved for select patients who need intensive care unit management or are otherwise at
high risk. Stress ulcer prophylaxis is reasonable for patients who have risk factors such as
intensive care unit stay lasting >1 week, mechanical ventilation for >48 hours, sepsis,
hereditary or acquired coagulopathy, including therapeutic anticoagulation, a history of GI
ulceration or bleeding within the past year, occult gastrointestinal bleeding lasting ≥6 days, or
treatment with high-dose glucocorticoids. (See "Stress ulcers in the intensive care unit:
Diagnosis, management, and prevention", section on 'High risk patients'.)
There is some evidence that enteral nutrition alone may reduce the risk of overt GI bleeding
due to stress ulceration and that stress ulcer prophylaxis may be ineffective or harmful among
patients who are receiving enteral nutrition, as reviewed separately. (See "Stress ulcers in the
intensive care unit: Diagnosis, management, and prevention", section on 'High risk patients'.)
● Management – Withholding of antiplatelet or anticoagulant therapy in the setting of clinically

overt GI bleeding should be individualized. The management of GI bleeding is discussed in
detail elsewhere. (See "Approach to acute upper gastrointestinal bleeding in adults" and
"Approach to acute lower gastrointestinal bleeding in adults" and "Evaluation of occult
gastrointestinal bleeding".)

Urinary incontinence — Urinary incontinence is a common problem after stroke and is

associated with poor functional outcome and mortality, perhaps because it is a marker of stroke
severity [66-70]. Urinary incontinence is present in 32 to 79 percent of patients on admission, and
25 to 28 percent at discharge [71]. Data from prospective population-based studies suggest that in
previously continent patients, new urinary incontinence is found in 35 to 40 percent of patients at 7
to 10 days after acute stroke [70]. The prevalence of poststroke incontinence decreases with time.
Of a group of 95 patients with incontinence 7 to 10 days after stroke, incontinence persisted at
three months, one year, and two years in 36, 24, and 13 percent, respectively [72].
The most frequent urodynamic finding is detrusor hyperreflexia [73]. The loss of inhibitory input
from higher neurologic centers is thought to cause this hyperreflexia leading to urinary urgency,
frequency, and urge incontinence. In addition to detrusor hyperreflexia, detrusor hyporeflexia or
areflexia may also occur following stroke, leading to overflow incontinence. Detrusor-sphincter
dyssynergia is an uncommon phenomenon in patients with recent stroke, unlike other neurologic
disorders associated with incontinence.
● Risk factors – Risk factors for the development of urinary incontinence in patients with stroke
include hemiparesis, depression, cognitive impairment, age >75 years, dysphagia, visual field
defect, and large infarcts (cortical plus subcortical area involvement) [74,75]. Other factors
contributing to urinary retention include the use of anticholinergic drugs, diabetic cystopathy,
and bladder outlet obstruction.
● Prevention – Indwelling bladder catheter placement should be avoided when possible to

decrease the risks of nosocomial infection, which is a potential contributing factor for urinary
incontinence.
● Evaluation and management – Practitioners can easily overlook urinary incontinence if

patients or nursing staff are not directly queried. Diagnosis of the type of incontinence and
appropriate treatment can be coordinated with a urologist. Detrusor hyperreflexia can be
treated with scheduled voiding, tailored fluid restriction, and anticholinergic drugs. There is
little evidence to support specific interventions for urinary incontinence after stroke [76]. The
evaluation and treatment of urinary incontinence is discussed in detail separately. (See
"Urinary incontinence in men" and "Evaluation of women with urinary incontinence" and
"Treatment of urinary incontinence in women".)
Falls and bone fractures — Falls have been cited as the one of the most common complications
of acute stroke [1,77]. In a prospective multicenter study of 311 patients followed up to 30 months
after stroke, falls occurred in 25 percent and were associated with serious injury in 5 percent [1].
Hip fractures represent 45 percent of poststroke fractures and are two to four times more common
in the population with stroke compared with an age-matched reference population [78]. A
retrospective case-control study found that the rate of falls among hospitalized patients with acute
ischemic stroke was only 2.3 percent [79].
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Hospitalized patients with stroke not only have skeletal "unloading" secondary to bed rest, but they
also have disuse of the paretic limbs. These factors predispose patients to bone resorption.
Patients who are able to ambulate early after stroke appear to lose bone density only on the
paretic side (hemiosteoporosis), while those who are not ambulatory lose bone mineral density on
both sides. Relearning to walk by two months has been associated with diminished bone density
loss compared with remaining wheelchair bound [80].
● Risk factors – Patients with cognitive impairment, neglect, anosognosia, and/or

polypharmacy may be at especially high risk for falls [19]. Most fractures after stroke occur on
the paretic side and are secondary to accidental falls [78,81]. Poststroke patients tend to fall
toward the paretic side and lack ample protective responses, such as outstretching an arm,
putting them at higher risk for fractures. (See "Falls in older persons: Risk factors and patient
evaluation".)
● Prevention – Fall precautions should be implemented for all patients with acute stroke;
specific elements include measures to reduce the risk of delirium, the use of bed and chair
alarms, minimal use of mechanical restraints, and use of ceiling lifts to assist with transfers
[19]. However, the evidence supporting these measures for fall prevention in patients with
stroke is limited [82].
Depression — Poststroke depression is common, although difficult to quantify precisely due to

methodologic differences among studies. A 2013 meta-analysis, with pooled data from 43 studies
and over 20,000 patients, found that the prevalence of depression observed at any time after
stroke was 29 percent (95% CI 25-32 percent) [83]. There was no significant difference in
prevalence rates of depression at different time points after stroke. In pooled data from 10 studies
with over 16,000 patients, predictors of poststroke depression were disability, prestroke
depression, cognitive impairment, stroke severity, and anxiety.
In a later case-control study that compared over 135,000 patients with stroke and no diagnosis of
depression at baseline with 145,000 matched controls, the incidence of depression during the first
two years after hospitalization was significantly higher for the group with stroke (25 versus 8
percent) [84].
Depression after stroke is correlated with a poorer functional outcomes [85], although causation
cannot be inferred from this. Nonetheless, when patients are matched for initial functional
outcome, remission of depression is associated with a better functional outcome at three and six
months than continued depression [86]. There appears to be a relationship between depression
and 12- and 24-month mortality, but confounders likely exist [87].
The theory that depression is more commonly associated with left than with right hemisphere
strokes and with lesions of the left anterior brain than with other regions [88] is not supported by
the data. In a systematic review of 48 studies, the relative risk of depression after a left versus

right hemisphere stroke was 0.95 (95% CI 0.83-1.10) [89]. Similarly, the risk of depression after a
left anterior lesion compared with all other brain lesions was 1.17 (0.87-1.62).
● Risk factors – Possible risk factors for poststroke depression include physical disability,
stroke severity, prestroke depression, cognitive impairment, and insufficient family and social
support [85].
● Prevention – It is unclear whether interventions to prevent poststroke depression are

warranted. A 2008 systematic review identified 14 trials involving 1515 subjects that
evaluated prevention of poststroke depression [90]. In 10 trials of pharmacological therapy,
there was no clear benefit. In four trials testing psychotherapy, there was a statistically
significant benefit for prevention of depression, but the treatment effects were small. In a later
controlled trial of 176 patients without depression who were within three months of acute
stroke, escitalopram was superior to placebo over 12 months of treatment for the prevention
of poststroke depression [91].
Further study in rigorous clinical trials is needed to determine the utility of antidepressant
interventions for preventing depression after acute stroke.
● Assessment – There are many depression scales that can be used to assess depression
after stroke. The single question "Do you often feel sad or depressed?" was found to have a
sensitivity and specificity of 86 and 78 percent, respectively when used against the
Montgomery-Asberg depression rating in screening for poststroke depression [92]. (See
"Unipolar depression in adults: Assessment and diagnosis".)
● Treatment – Major depression is a treatable illness that responds to a variety of therapeutic

interventions, and it is likely that the standard approach to the treatment of depression in
adults is generalizable to patients with poststroke depression. The initial treatment of
depression is discussed separately. (See "Unipolar major depression in adults: Choosing
initial treatment".)
There is no definitive evidence to guide the specific choice of therapy for patients with
poststroke depression [85]. The effectiveness of pharmacotherapy, psychotherapy, or
combined use of these modalities for poststroke depression is not established, but
accumulating evidence suggests that these interventions are beneficial.
Poststroke fatigue — Poststroke fatigue lacks a consensus definition, but encompasses a

subjective feeling of exhaustion and lack of physical or mental energy and/or an increased need
for rest that interferes with usual activities [93,94]. It is generally distinguished from poststroke
depression, although the two may exist concurrently. The pathophysiology of poststroke fatigue is
unsettled; possible factors include disturbances in cortical excitability, inflammation, and genes
that modulate inflammation [93,95,96].

The prevalence of poststroke fatigue ranges from 23 to 75 percent in different studies [97]; the
wide range is likely due to variation in definitions, patient populations, assessment scales, and
time points (most often six months after stroke onset) among different reports [93]. Some studies
distinguish between early poststroke fatigue (up to two to three months after stroke onset) and late
poststroke fatigue (more than three months after stroke onset) [95,96,98]. However, it is unclear
whether these two phases of fatigue are distinct [95].
There is no consensus about the need to screen for poststroke fatigue, and no proven therapy is
available [99]. In a randomized trial of 36 patients with poststroke fatigue more than three months
after stroke, modafinil was more effective than placebo for reducing fatigue and improving quality
of life [100], but definitive conclusions are precluded by the small size of the trial, and further study
is needed. Other suggested interventions for poststroke fatigue include promoting physical activity
and exercise, identifying and treating depression, anxiety, pain, and sleep disturbances, and
avoiding sedating drugs and excessive alcohol [93,94],
NEUROLOGIC COMPLICATIONS
Intracranial complications — Intracranial complications of acute stroke include the development

of cerebral edema, symptomatic hemorrhagic transformation of ischemic stroke, elevated
intracranial pressure, and hydrocephalus. Cerebral edema with space-occupying mass effect
develops in a minority of ischemic stroke, but can cause neurologic deterioration and life-
threatening herniation.
The clinical features and management of intracranial complications of stroke are reviewed
separately for each major type of stroke:
● Ischemic stroke (see "Malignant cerebral hemispheric infarction with swelling and risk of
herniation")
● Intracerebral hemorrhage (see "Spontaneous intracerebral hemorrhage: Treatment and
prognosis")
● Subarachnoid hemorrhage (see "Aneurysmal subarachnoid hemorrhage: Treatment and
prognosis")
The general management of elevated intracranial pressure is discussed elsewhere. (See

"Evaluation and management of elevated intracranial pressure in adults".)
Neurologic deterioration — Early neurologic deterioration after stroke is associated with poor
outcome. The mechanisms of early neurologic deterioration are heterogeneous. Common causes
include infarct growth of ischemic stroke, hematoma expansion of intracerebral hemorrhage,
delayed cerebral ischemia associated with subarachnoid hemorrhage, other intracranial
complications (eg, progressive cerebral edema, hemorrhagic transformation of ischemic stroke)
and toxic-metabolic encephalopathy due to medical complications (eg, concomitant infection;
cardiovascular, pulmonary, and/or renal dysfunction). Interventions that address the underlying
cause may help to improve outcome. However, the cause of early neurologic deterioration is often
unclear.
Seizures — Early seizures after stroke are relatively uncommon but are associated with poor
outcome. Risk factors include worse stroke severity and cortical involvement. Poststroke seizures
are reviewed elsewhere. (See "Overview of the management of epilepsy in adults", section on
'Poststroke seizures'.)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Stroke in adults".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Stroke (The Basics)" and "Patient education: Recovery
after stroke (The Basics)")
● Beyond the Basics topics (see "Patient education: Stroke symptoms and diagnosis (Beyond
the Basics)")
SUMMARY AND RECOMMENDATIONS
● Medical complications after ischemic stroke are common (table 1 and table 2) and influence
outcome. Potentially serious complications include pneumonia, urinary tract infection,
gastrointestinal bleeding, myocardial infarction, deep vein thrombosis, and pulmonary
embolism. (See 'Medical complications' above.)

● We evaluate swallowing function using a water swallow test at the time of admission for all
patients with acute stroke before administering oral medications or food. Prevention of
aspiration in patients with dysphagia includes initial nil per os (NPO) status for those who may
be at risk for aspiration and subsequent dietary modifications for those who have persistent
dysphagia. Patients with acute stroke who cannot take food and fluids orally should receive
nutrition and hydration via nasogastric, nasoduodenal, or percutaneous endoscopic
gastrostomy tube feedings while undergoing efforts to restore swallowing. (See 'Dysphagia'
above.)
● VTE prophylaxis is indicated for all patients with acute stroke who have restricted mobility, as
reviewed separately. (See "Prevention and treatment of venous thromboembolism in patients
with acute stroke".)
● Pneumonia and urinary tract infection are the two most common infectious complications of
acute stroke. Screening on admission for swallowing difficulty is an important measure to
prevent pneumonia in patients with acute stroke, as discussed above. Measures to prevent
aspiration pneumonia in patients with dysphagia include initial nil per os (NPO; nothing by
mouth) status and subsequent dietary modifications for those who have persistent dysphagia.
Placement of an indwelling bladder catheter is an important risk factor for urinary tract
infection and should be avoided if possible. (See 'Pneumonia' above and 'Urinary tract
infection' above.)
● Myocardial infarction, cardiac arrhythmias, and neurogenic cardiac injury are potential
complications of acute stroke. All patients with acute stroke should have electrocardiography
(ECG) and troponin level on admission, and continuous cardiac monitoring at least the first 24
hours of admission. (See 'Cardiac complications' above.)
● Besides pneumonia, serious pulmonary complications of stroke include neurogenic

pulmonary edema and the need for intubation and mechanical ventilation. (See 'Pulmonary
complications' above.)
● Gastrointestinal (GI) bleeding is one of the more common complications of acute stroke. Risk
factors include older age, severe stroke, and a history of peptic ulcer disease or cancer
predating the incident stroke. GI stress ulcer prophylaxis with proton pump inhibitors or
histamine-2 antagonists is not used routinely for patients with acute stroke, but is reserved for
select patients who need intensive care unit management. (See 'Gastrointestinal bleeding'
above.)
● Urinary incontinence after stroke is associated with poor functional outcome and mortality,
perhaps because it is a marker of stroke severity. in previously continent patients, new urinary
incontinence is found in 35 to 40 percent of patients at 7 to 10 days after acute stroke. The

prevalence of poststroke incontinence decreases with time. (See 'Urinary incontinence'

above.)
● Falls after acute stroke and are associated with serious injury in 5 percent of patients. Fall
precautions should be implemented for all patients with stroke, particularly those with
hemiparesis, cognitive impairment, neglect, anosognosia, and/or polypharmacy. (See 'Falls
and bone fractures' above.)
● The prevalence of poststroke depression is 18 to 61 percent. Stroke severity, physical

disability, and cognitive impairment are likely risk factors. The effectiveness of
pharmacotherapy, psychotherapy, or combined use of these modalities for poststroke
depression is not established, but accumulating evidence suggests that these interventions
are beneficial. Thus, the standard approach to the treatment of depression is likely to be
generalizable to patients with poststroke depression. (See 'Depression' above.)
● Neurologic complications of acute stroke encompass intracranial morbidities (progressive

cerebral edema, symptomatic hemorrhagic transformation of ischemic stroke, elevated
intracranial pressure, hydrocephalus), neurologic deterioration, and (uncommonly) seizures.
(See 'Neurologic complications' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate, Inc. would like to acknowledge Dr. Teresa Jacobs, who contributed
to earlier versions of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 1093 Version 33.0

GRAPHICS
Common medical complications of stroke
Complication Percent
Falls 25
Urinary tract infection 24
Chest infection 22
Pressure sores 21
Depression 16
Shoulder pain 9
Deep venous thrombosis 2
Pulmonary embolism 1
Medical complications of stroke were frequent in a prospective multicenter study of 311 patients followed weekly through
hospital discharge and again at 6, 18, and 30 months after stroke.
Data from: Langhorne, P, Stott, DJ, Robertson, L, et al. Medical complications after stroke: a multicenter study. Stroke
2000; 31:1223.
Graphic 52076 Version 2.0

Serious medical complications of stroke
Complication Percent
All pneumonias 5
Aspiration pneumonia alone 3
Heart failure 3
Gastrointestinal bleeding 3
Cardiac arrest 2
Angina/MI/cardiac ischemia 1
Deep venous thrombosis 1
Pulmonary embolism 1
Hypoxia 1
Urinary tract infection 1
Sepsis 1
Cellulitis 1
Peripheral vascular disorder 1
Dyspnea 1
Pulmonary edema 1
Dehydration 1
In a prospective study that analyzed the placebo group of the RANTTAS database (n = 279), at least one serious
medical complication (defined as prolonged, immediately life threatening, or resulting in hospitalization or death)
occurred in 24 percent of patients.
Data from: Johnston, KC, Li, JY, Lyden, PD, et al. Medical and neurological complications of ischemic stroke: experience
from the RANTTAS trial. RANTTAS Investigators. Stroke 1998; 29:447.

Causes of elevated troponin
Myocardial ischemia
Acute coronary syndrome
STEMI
NSTEMI
Other coronary ischemia
Arrhythmia: tachy- or brady-
Cocaine/methamphetamine use
Coronary intervention (PCI or cardiothoracic surgery)
Coronary artery spasm (variant angina)
Stable coronary atherosclerotic disease in setting of increased O 2 demand (eg, tachycardia)
Severe hypertension
Coronary embolus
Aortic dissection
Coronary artery vasculitis (SLE, Kawasaki)
Non-coronary ischemia
Shock (hypotension)
Hypoxia
Hypoperfusion
Pulmonary embolism
Global ischemia
CT surgery
Myocardial injury with no ischemia

Comorbidities
Renal failure
Sepsis
Infiltrative diseases
Acute respiratory failure
Stroke
Subarachnoid hemorrhage
Specific identifiable precipitants
Extreme exertion
Cardiac contusion
Burns >30% BSA
Cardiotoxic meds: anthracyclines, herceptin
Electrical shock
Carbon monoxide exposure
Other
Apical ballooning (Takotsubo)
Myocarditis
Myopericarditis
Rhabdomyolysis involving cardiac muscle
Hypertrophic cardiomyopathy

Peripartum cardiomyopathy
Heart failure, malignancy, stress cardiomyopathy
BSA: body surface area; CT: cardiothoracic; NSTEMI: non-ST elevation myocardial infarction; PCI: percutaneous coronary
intervention; SLE: systemic lupus erythematosus; STEMI: ST elevation myocardial infarction.

Causes of neurogenic pulmonary edema
Major causes
Epileptic seizures, particularly status epilepticus
Intracranial hemorrhage (including intracerebral hemorrhage, intraventricular hemorrhage, epidural hemorrhage,

subdural hemorrhage)
Head injury
Minor causes
Guillain-Barré syndrome
Multiple sclerosis with medullary involvement
Nonhemorrhagic strokes
Trigeminal nerve block
Bulbar poliomyelitis
Vertebral artery ligation
Vertebral artery dissection
Ruptured spinal arteriovenous malformation
Air embolism
Brain tumors
Electroconvulsive therapy
Induction of general anesthesia
Colloid cyst
Hydrocephalus
Reye syndrome
Bacterial meningitis
Viral meningoencephalitis (including enterovirus-7)
Cervical spinal cord injury
Cryptococcal meningoencephalitis
Hyponatremia
Electroconvulsive therapy

Respiratory patterns associated with neurological injury

Contributor Disclosures
Koto Ishida, MD Nothing to disclose Scott E Kasner, MD Grant/Research/Clinical Trial Support: WL Gore
and Associates [Stroke (PFO closure)]; Bayer [Stroke (rivaroxaban)]; Bristol Meyers Squibb [Stroke];
Medtronic [Stroke]. Consultant/Advisory Boards: Bayer; BMS; Merck; Boehringer Ingelheim; Abbvie; J&J;
Medtronic; Urovant; Janssen [Stroke]. John F Dashe, MD, PhD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
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These observations are supported by a systematic review of 24 studies that evaluated

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Venous thromboembolism — Venous thromboembolism (VTE) encompasses deep vein

Pneumonia — Pneumonia develops in 4 to 10 percent of patients with acute stroke

Aspiration is the cause of about 60 percent of post-stroke pneumonia [2]. Aspiration

● Prevention — Measures to prevent aspiration pneumonia in patients with dysphagia include

Screening on admission for swallowing difficulty is an important measure to prevent

● Diagnosis and management – The diagnosis and management of hospital acquired

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Cardiac complications — Myocardial infarction, cardiac arrhythmias, and neurogenic cardiac

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Pulmonary complications — Serious pulmonary complications of stroke include pneumonia,

● Neurogenic pulmonary edema – Neurogenic pulmonary edema (NPE) is reviewed here

● Abnormal respiratory patterns – Abnormal respiratory patterns may complicate stroke;

Sleep-related breathing disorders — The relationship of sleep-disordered breathing (including

Gastrointestinal bleeding — Gastrointestinal (GI) hemorrhage affects 1.5 to 3 percent of patients

● Prevention – GI stress ulcer prophylaxis with proton pump inhibitors or H2 antagonists is

● Management – Withholding of antiplatelet or anticoagulant therapy in the setting of clinically

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Urinary incontinence — Urinary incontinence is a common problem after stroke and is

● Prevention – Indwelling bladder catheter placement should be avoided when possible to

● Evaluation and management – Practitioners can easily overlook urinary incontinence if

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● Risk factors – Patients with cognitive impairment, neglect, anosognosia, and/or

Depression — Poststroke depression is common, although difficult to quantify precisely due to

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● Prevention – It is unclear whether interventions to prevent poststroke depression are

● Treatment – Major depression is a treatable illness that responds to a variety of therapeutic

Poststroke fatigue — Poststroke fatigue lacks a consensus definition, but encompasses a

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Intracranial complications — Intracranial complications of acute stroke include the development

The general management of elevated intracranial pressure is discussed elsewhere. (See

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● Besides pneumonia, serious pulmonary complications of stroke include neurogenic

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prevalence of poststroke incontinence decreases with time. (See 'Urinary incontinence'

● The prevalence of poststroke depression is 18 to 61 percent. Stroke severity, physical

● Neurologic complications of acute stroke encompass intracranial morbidities (progressive

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3. Indredavik B, Rohweder G, Naalsund E, Lydersen S. Medical complications in a

4. Ingeman A, Andersen G, Hundborg HH, et al. In-hospital medical complications, length of

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36. Khechinashvili G, Asplund K. Electrocardiographic changes in patients with acute stroke: a

38. Fernández-Menéndez S, García-Santiago R, Vega-Primo A, et al. Cardiac arrhythmias in

42. Samuels MA. The brain-heart connection. Circulation 2007; 116:77.

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51. Ay H, Koroshetz WJ, Benner T, et al. Neuroanatomic correlates of stroke-related myocardial

54. Meyer S, Strittmatter M, Fischer C, et al. Lateralization in autonomic dysfunction in ischemic

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85. Towfighi A, Ovbiagele B, El Husseini N, et al. Poststroke Depression: A Scientific Statement

94. Paciaroni M, Acciarresi M. Poststroke Fatigue. Stroke 2019; 50:1927.

95. De Doncker W, Dantzer R, Ormstad H, Kuppuswamy A. Mechanisms of poststroke fatigue. J

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