Version May 2024
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.
The prognosis of stroke is reviewed separately:
●(See "Overview of ischemic stroke prognosis in adults".)
●(See "Lacunar infarcts", section on 'Prognosis'.)
●(See "Intracranial large artery atherosclerosis: Treatment and prognosis", section on 'Prognosis'.)
●(See "Cryptogenic stroke and embolic stroke of undetermined source (ESUS)", section on 'Prognosis'.)
●(See "Stroke after cardiac catheterization", section on 'Prognosis'.)
●(See "Ischemic stroke in children: Management and prognosis", section on 'Prognosis'.)
●(See "Stroke in the newborn: Management and prognosis", section on 'Prognosis'.)
●(See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Early prognosis'.)
●(See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Prognosis'.)
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 and populations vary across studies, but improving care may be reducing some 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]. In an analysis from the United States of the 2007-2019 National Inpatient Sample database of over 5,750,000 adults admitted with a primary diagnosis of acute ischemic stroke, infectious complications decreased while noninfectious complications increased over the study period [7].
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) [8].
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 [9]. 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.
These observations are supported by a systematic review of 24 studies that evaluated oropharyngeal dysphagia and aspiration in adult patients with stroke [9]. 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) [9]. 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 facial palsy, aphasia, age greater than 70, stroke severity (higher scores on the National Institutes of Health Stroke Scale [NIHSS]), impaired pharyngeal response, incomplete oral clearance, and palatal weakness or asymmetry [10-12]. Dysphagia usually improves spontaneously with return of safe swallowing function by two weeks in approximately 90 percent of patients [9,13,14]. 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 [15]. The water swallow test is simple and quick to perform, although the specific method of testing can vary in different stroke centers. The patient, who must be awake and alert, is positioned upright in bed as high as tolerated between 30 to 90 degrees and instructed to drink 3 ounces (90 cc) of water from a cup by mouth (use of a straw is permitted) slowly and steadily without stopping [16-18]. The test is passed if the patient can drink the entire volume of water without coughing or choking during or immediately (eg, within one minute) after swallowing. The test is failed if the patient develops coughing, choking, gurgling, or is unable to drink the entire volume of water in a single or sequential swallows.
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) [19]. 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 [20-22]. 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 [21]. 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 [23]. 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 [24].
●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 [25]. (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 [26]. 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 [27]. 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 intubated critically ill adult patients: Initial evaluation and prescription" 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".)
Fever and infection
Burden of fever — Fever is a common complication of stroke, may worsen outcomes, and can sometimes lead to clinically nonindicated and potentially harmful antimicrobial use. In one retrospective report of 1361 patients hospitalized with acute ischemic stroke, one or more episodes of fever affected approximately 36 percent of patients [28].
●Effect on outcomes – Fever is associated with unfavorable outcomes in human studies of stroke [28-31]. In a meta-analysis of over 14,000 patients with neurologic injury, including hemorrhagic and/or ischemic stroke, fever was associated with increased mortality rates, greater disability, more dependence, worse functional outcome, greater severity, and longer intensive care unit and hospital stays [29]. These results were consistent for overall pooled data and for subgroups limited to studies of patients with hemorrhagic, ischemic, or all stroke types. A subsequent meta-analysis found that fever within 24 hours of hospital admission in patients with ischemic stroke was associated with a two-fold increase in the odds of mortality at one month after stroke onset [31].
Fever may contribute to brain injury in patients with an acute stroke. This concept has been demonstrated in animal models in which ischemic injury is increased in the presence of elevated temperature. Hyperthermia may act via several mechanisms to worsen cerebral ischemia [32,33]:
•Enhanced release of neurotransmitters
•Exaggerated oxygen radical production
•More extensive blood-brain barrier breakdown
•Increased numbers of potentially damaging ischemic depolarizations in the focal ischemic penumbra
•Impaired recovery of energy metabolism and enhanced inhibition of protein kinases
•Worsening of cytoskeletal proteolysis
●Management – Temperature reduction to achieve normothermia is the preferred strategy for the management of fever. (See "Initial assessment and management of acute stroke", section on 'Fever'.)
Prophylactic antibiotics may reduce the rate of overall infection in patients with acute stroke but do not reduce mortality or improve functional outcome [34].
Pneumonia — Pneumonia develops in 3 to 10 percent of patients with acute stroke [4,6,7,35,36]. Stroke-related pneumonia is associated with a higher mortality and a poorer long-term outcome [4,35,37,38].
●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 [39-42].
Aspiration is the cause of approximately 60 percent of poststroke 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 [25]. 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 [43,44]. Several 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 [1,4,7] and constitutes a serious complication (ie, prolonged, immediately life threatening, or resulting in hospitalization or death) in approximately 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 measure of poststroke disability), and postvoid residual volume >100 mL [45].
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 [46].
●Prevention – The use of indwelling urinary catheters should be avoided whenever possible [15]. 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 test 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. Most 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'.)
Indwelling urinary catheters and older age are associated with an increased risk of asymptomatic bacteriuria. 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 adult and adolescent females" and "Acute simple cystitis in adult and adolescent males" and "Recurrent simple cystitis in women" and "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents".)
Cardiac complications — Myocardial infarction, cardiac arrhythmias, and neurogenic cardiac injury are potential short- and long-term complications of acute stroke [47].
Myocardial infarction — All patients with acute stroke should have electrocardiography (ECG) and troponin level on admission, and continuous cardiac monitoring for at least the first 24 hours of admission to detect arrhythmias, particularly atrial fibrillation [15,48]. Data from the modern era suggest that myocardial infarction (MI) occurs in approximately 1 to 2.5 percent of patients with acute stroke during initial hospitalization and is associated with poor outcome [2,6,7,49].
MI should be suspected in 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 [50], 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 pre-existing coronary disease [51].
●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 [52,53], 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 [54]. 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 [52]. 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 [55]. Some patients develop a pattern of transient apical left ventricular dysfunction that mimics myocardial infarction, but in the absence of significant coronary artery disease [56]. 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 [57,58]. 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 [59,60]. 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 [57]. The myofibrillar degeneration occurs in the vicinity of the cardiac nerves, and not in the macrovascular distribution seen in patients with coronary disease [57,61]. 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 [62-68]. The presumed biologic basis for this association is the role of the insular cortex in the autonomic control of cardiovascular function [63,67-75].
Acute kidney injury — In an analysis of the 2007-2019 National Inpatient Sample of over 5,750,000 adults admitted for acute ischemic stroke in the United States, the prevalence of acute kidney injury was approximately 10 percent, making it one of the most common complications [7]. Among patients on mechanical ventilation, the prevalence of AKI was approximately 25 percent.
Pulmonary complications — Serious pulmonary complications of stroke include pneumonia, neurogenic pulmonary edema, and the need for intubation and mechanical ventilation [76].
●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 initiating invasive mechanical ventilation in adults in the intensive care unit" and "Clinical and physiologic complications of mechanical ventilation: Overview", section on 'Increased intracranial pressure'.)
●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 1.1 to 3 percent of patients with acute stroke [2,7,77,78]. 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 [77-80].
●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 more than one 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 [81-85]. Urinary incontinence is present in 32 to 79 percent of patients on admission, and 25 to 28 percent at discharge [86]. 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 [85]. 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 [87].
The most frequent urodynamic finding is detrusor hyperreflexia [88]. 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) [89,90]. 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 [91]. The evaluation and treatment of urinary incontinence is discussed in detail separately. (See "Urinary incontinence in men" and "Female urinary incontinence: Evaluation" and "Female urinary incontinence: Treatment".)
Falls and bone fractures — Falls have been cited as one of the most common complications of acute stroke [1,92,93]. 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 [94]. A retrospective case-control study found that the rate of falls among hospitalized patients with acute ischemic stroke was only 2.3 percent [95].
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 can 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 nonambulatory [96].
●Risk factors – Patients with cognitive impairment, neglect, anosognosia, and/or polypharmacy may be at especially high risk for falls [25]. Other risk factors for poststroke falls include a history of prior fracture or fall, malnutrition, depression, osteoarthritis, older age, and female sex [93].
Most fractures after stroke occur on the paretic side and are secondary to accidental falls [94,97]. 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 [25]. However, the evidence supporting these measures for fall prevention in patients with stroke is limited [98].
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) [99]. 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) [100].
Depression after stroke is correlated with poorer functional outcomes [101], 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 [102]. There appears to be a relationship between depression and 12- and 24-month mortality, but confounders likely exist [103].
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 [104] 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) [105]. 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 [101].
●Prevention – It is unclear whether interventions to prevent poststroke depression are effective. A 2020 systematic review identified 49 trials involving 3342 subjects that evaluated prevention of poststroke depression [106]. The review concluded that there was only very low certainty evidence that pharmacologic or psychologic therapies reduced the prevalence of poststroke depression.
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 [107]. (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 [101]. 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. For patients able to engage in physical activity, exercise may be helpful. (See "Unipolar major depression in adults: Choosing initial treatment".)
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 [108,109]. 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 [108,110,111].
The prevalence of poststroke fatigue ranges from 23 to 75 percent in different studies [112]; 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 [108]. 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) [110,111,113]. However, it is unclear whether these two phases of fatigue are distinct [110].
There is no consensus about the need to screen for poststroke fatigue, and no proven therapy is available [114]. 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 [115], 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 [108,109].
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: Acute 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".)
Early neurologic deterioration — Early neurologic deterioration (END) after acute stroke occurs in 2 to 38 percent of patients and is associated with poor outcomes [116-119]. The wide range in the frequency of END probably reflects differences in the patient populations studied and variations in the definitions of END.
The mechanisms of END are heterogeneous. Common causes include extension of the infarct into surrounding areas of hypoperfused brain tissue, 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) [116,120-122]. Interventions that address the underlying cause may help to improve outcome. However, the cause of END is often unclear [116].
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; nothing by mouth) 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 NPO 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 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 UpToDate editorial staff acknowledges Dr. Teresa Jacobs, who contributed to earlier versions of this topic review.
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