Medical Complications

Although the effectiveness of a stroke unit is largely based on optimal general care which largely consists of the prevention and treatment of complications, only few clinical trials have tested the effects of prevention and treatment of specific complications on patients with acute ischemic stroke.

Venous Thrombosis and Pulmonary Embolism

In an older study, deep venous thrombosis occurred in about 50% of the patients with severe stroke and was confined mainly to the paretic leg (46). Severe leg weakness, a shortened activated partial thromboplastin time (47), and atrial fibrillation (48) have been associated with an increased risk of deep venous thrombosis. The complication is feared mainly because of the risk of pulmonary embolism, which has an estimated incidence of about 1% (49).

Overall, prophylactic administration of unfractionated heparin, low molecular weight heparin, or heparinoid is associated with an 81% reduction in deep venous thrombosis as detected by I125 fibrinogen scanning or a venogram (50).

Compression stockings are recommended for patients who cannot receive anticoagulants. Although early mobilization is not an absolute guarantee against venous thromboembolism, patients should be mobilized as early as possible.

For stroke patients with deep venous thrombosis or pulmonary embolism, the use of therapeutic anticoagulation should be weighed against the risk of intracranial hemorrhagic complications. The use of a vena cava filter may be considered in patients with absolute contraindications to anticoagulation (22).


Between 5 and 10% of patients with ischemic stroke suffer from epileptic seizures in the first week and about 3% within the first 24 h (51, 52). Early seizures are more often partial than generalized and status epilepticus is uncommon. Most seizures occur in patients with cardioembolic stroke and in patients with cortical involvement (52). Acute seizures are associated with a higher mortality at 30 days after stroke, but seizures are not an independent risk factor of mortality at 30 days after stroke (52). Post-stroke seizures are not associated with a higher mortality or worse functional outcome. The natural history of early seizures after stroke is unknown, as most patients are promptly treated with anticonvulsants. About 1 out of every 11 patient with an early epileptic seizure develops epilepsy within 10 years after stroke onset (51).

In case of a seizure in the acute phase of stroke, administration of anticonvulsant drugs to prevent recurrent seizures has been recommended, although this is not evidence based. In case of an early seizure without recurrences the anticonvulsants can probably be stopped after the first weeks.


In the first 12 h after stroke onset, plasma glucose concentrations are elevated in up to 68% of patients, of whom more than half are not known to have diabetes mellitus (53). An initially high blood glucose concentration in patients with acute stroke is a predictor of poor outcome (53, 54). Lowering blood glucose in the acute stage of ischemic stroke has been in only one phase III clinical trial that was terminated prematurely. This trial did not show a benefit on long-term functional outcome of early administration of insulin, but the reduction in serum glucose achieved was only small (55). For more information on hyperglycemia in the acute phase of stroke, the reader is referred to Treatment of Hyperglycemia, Chapter 9.


Acute stroke is associated with a blood pressure higher than 170/110 mmHg in about two thirds of patients. Blood pressure falls spontaneously in the majority of patients during the first week after stroke. High blood pressure during the acute phase of stroke has been associated with a poor outcome (56).

It is unclear how blood pressure should be managed during the acute phase of ischemic stroke. Randomized trials are needed to determine the effect of lowering blood pressure in the acute stage of stroke. Meanwhile, routine lowering of the blood pressure is not recommended in the first week after stroke, except for extremely elevated values on repeated measurements (systolic pressure >220 mmHg or diastolic pressure >120 mmHg) or in patients with cardiac ischemia, cardiac failure, or dissection of the aorta. In patients who have elevated blood pressure and are otherwise eligible for intravenous or intra-arterial thrombolysis, very careful management of blood pressure is necessary, at least during the first 24 h. If systolic blood pressure rises above 185 mmHg or if diastolic blood pressure rises above 110 mmHg, hypertension should be treated by means of intravenous labetalol or, in refractory cases, by means of intravenous sodium nitroprus-side (22).


Swallowing difficulties have been found in 27-50% of the patients in the first days after stroke (57). Although dysphagia is more common in patients with lower brain stem lesions it is found on admission in one third of conscious patients with unilateral hemispheric stroke, especially when aphasia and facial weakness are present. In most patients, dysphagia resolves spontaneously by the end of the first week, and at 1 month only a minority of survivors still has swallowing problems (58). Patients with impaired swallowing have a high risk of aspiration and chest infection and a poor nutritional state. Dysphagia is associated with an increased risk of death and poor functional outcome (57).

Swallowing of a small amount of water is the best early screening tool for dysphagia, but sometimes fiber optic endoscopy is necessary to assess safety of swallowing (57). A Cochrane Review did not find any benefit from swallowing therapy in the acute stage of stroke (59). In dysphagic stroke patients, no statistically significant effects on long-term functional outcome were observed from early tube feeding or early percutaneous endoscopic gastrostomy (PEG) feeding (60).

Pressure Sores

During the first week after stroke onset, pressure sores are rare. They have been found in less than 1% of patients treated in a stroke unit (49), but in 27% of stroke patients in long-term units (61). Pressure sores can cause considerable pain and usually slow the patient's recovery. Immobilization is the most important cause. Previous stroke, previous trauma, and cognitive decline are also associated with an increased risk of pressure sores (61). Prevention relies on an early and accurate assessment of the risk to develop pressure sores. Prevention should include regular turning of the patient, relief of bony prominences, early mobilization, and adequate nutrition (62).

Bladder Dysfunction

Urinary incontinence affects up to 60% of stroke patients admitted to hospital, with 25% still having problems on hospital discharge, and around 15% remaining incontinent at 1 year. The most common cause is detrusor hyper-reflexia as a direct consequence of stroke. Impaired sphincter control, preexisting bladder outflow obstruction, constipation, immobility, confusion, impaired consciousness, and urinary tract infection may also play a role (63).

Data from the available trials are insufficient to guide continence care after stroke. It has been suggested that structured assessment and management of care and specialist continence nursing may reduce urinary incontinence and related symptoms after stroke (63). Nursing strategies, such as scheduled voiding, intermittent catheterization, or the use of condom catheters in men, are useful first-line treatments (64). Whenever possible, indwelling catheters should be avoided because of the risk of urinary tract infections. When incontinence persists, urodynamic studies are helpful in establishing the cause. After urological consultation, refractory bladder hyperreflexia can be treated with anticholinergic or antispasmodic medications and overflow incontinence with cholinergic drugs (64).


Between 22 and 43% of patients develop fever or subfebrile temperatures during the first days after stroke (42, 65). In most cases, pulmonary or urinary tract infections are the cause (66), but fever may also exist without signs of an overt infection (42, 65). Fever is more common in patients with larger infarcts (65). High body temperature in the first days after stroke is associated with poor outcome (42, 67). There is currently no evidence from randomized trials to support the routine lowering of body temperature above 37°C. Until data from the randomized Paracetamol (Acetaminophen) In Stroke Trial (68) become available, at least the source of fever should be determined and treated, and antipyretics may be given to patients with a body temperature of more than 38°C.

Mood Disorders

Up to 40% of patients develop depressive symptoms in the first 3 weeks after stroke, of which about a quarter are diagnosed as having a major depression (69). There is probably no relation between the location of the stroke and the risk to develop depression. Post-stroke depression is associated with an increased risk of poor functional outcome and a reduced quality of life (70).

Post-stroke depression may be treated with a serotonin reuptake inhibitor or in case of insufficient response with a tricyclic antidepressant (71). Unfortunately, mood disorders are often not recognized in stroke patients and are therefore too often left untreated.


The incidence of delirium after stroke has been reported between 13 and 48%. Delirium is more common after stroke than after myocardial ischemia, suggesting a causal relation between brain damage and the occurrence of delirium (72). Specific stroke types, such as large supratentorial infarcts, may be more likely to precipitate delirium than others. In addition, case reports have suggested that delirium may be associated with specific lesions in the thalamus and caudate nucleus (73). Age, pre-existing cognitive impairment or dementia, psychiatric disease, severe chronic medical illness, social isolation, previous delirium, poor vision, severe acute illness, polypharmacy, and treatment on an intensive care unit all precipitate delirium. Moreover, extensive motor impairment, neglect, and impaired vision are associated with a higher risk to develop delirium. In stroke patients, delirium is associated with a worse functional outcome, a higher mortality, a longer stay in the hospital, and an increased incidence of post-stroke dementia (72).

No trials concerning treatment of delirium in acute stroke have been performed. Therefore, prevention and treatment of delirium after stroke is not evidence based and recommendations are similar to management of delirium in patients with other diseases. General management should include identification and elimination of precipitating factors. Haloperidol is the drug most frequently used, because of minor anticholinergic effects, few active metabolites, and a small chance of sedation and hypotension. Risperidone and olanzapine may be safer than haloperidol, but experience with these drugs in the treatment of delirium after stroke is limited (72).

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