General Stroke Therapy | Acute Treatment | Treatment

In all stroke patients neurological status and vital functions should be continuously or discontinuously monitored. Neurological status is best monitored using validated neurological scales, such as the National Institutes of Health Stroke Scale (NIHSS), the Scandinavian Stroke Scale, the Glasgow Coma Scale and others.

	Respiratory / Cardiac monitoring and care Normal respiratory function and adequate blood oxygenation are essential to preserve metabolic function in the ischaemic penumbra

	Blood pressure control No randomized controlled trial (RCT) is available to guide blood pressure(BP) management in acute stroke. In the absence

	Fluid and electrolyte balance

	Control of glucose metabolism

	Treatment of fever

	Managment of dysphagia, and appropriate nutrition

References:
The European Ad Hoc Consensus Group. Cerebrovasc Dis 1996; 6: 315-324.
The European Ad Hoc Consensus Group. Cerebrovasc Dis 1997; 7: 113-128.

Respiratory Monitoring and Care

Normal respiratory function and adequate blood oxygenation are essential to preserve metabolic function in the ischaemic penumbra. However, there is no convincing prospective clinical evidence that oxygen supply at low flow rates is useful in human brain infarction, and hence routine oxygen administration to all acute stroke patients is not required.

Most common causes of hypoxaemia in stroke

Previous pulmonary diseases
Airway obstruction (vomiting, oropharingeal muscular hypotonia)
Acute aspiration (brainstem stroke; reduced vigilance)
Hypoventilation due to: large hemispheric infarct or haemorrhage, brainstem infarct or haemorrhage; status epilepticus; heart failure; pulmonary embolism

But acute stroke patients may be or may become hypoxic as a result of brainstem infarct or haemorrhage, or of brainstem compression by extensive hemispheric haemorrhage or infarct, or as a result of complications such as exacerbation of a chronic obstructive airway disease, mechanical airway obstruction (vomiting, oropharingeal muscle hypotonia), bronchopneumonia (particularly in patients at risk of aspiration), heart failure, pulmonary embolism, or sustained seizure activity.

Continuous monitoring with pulse oximetry or discontinuous checks with repeat blood gas analysis (BGA) should be done in patients with either severe stroke or impaired pulmonary function since hospital admission. Ventilation may be particularly compromised during sleep, with episodes of sleep apnoea or hypopnoea.

If there is no pathological respiratory pattern, and pulse oximetry or BGA reveal only moderate hypoxaemia (oxygen saturation < 92%), oxygen administration is sufficient. Non-invasive continuous positive airway pressure via nasal or facial mask might be used in patients with obstructive sleep apnoea, though its efficacy should be tested more accurately.

Consider intubation in case of:

Severe pre-existing and/or acute pulmonary disease
Acute aspiration
Impaired level of consciousness with risk of aspiration
Loss of caudal brainstem reflexes

Early endotracheal intubation may be useful in patients with a pathological respiratory pattern, severe hypoxaemia or hypercarbia, an impaired level of consciousness at high risk for aspiration, and in those with lost caudal brainstem reflexes. Before intubation, the general prognosis, co-existing life-threatening medical conditions and the presumed will of the patient and their family must be taken into account.

References:
Ronning et al. Stroke 1999; 30 (10): 2033-2037.
Iranzo et al. Neurology 2002; 58 (6): 911-916.
Turkington et al. Stroke 2002; 33 (8): 2037-2042.
Grotta et al. Neurology 1995; 45 (4): 640-644.

Blood Pressure Management

No randomized controlled trial (RCT) is available to guide blood pressure(BP) management in acute stroke. In the absence of such evidence, at present, recommendations on BP treatment give absolute treatment and target levels, though the effects of drugs on BP and events are relative and not absolute. The general approach is to treat systolic BP (SBP) values over 200 mm Hg or diastolic BP (DBP) values above 110 mm Hg in repeated measurements.

Immediate antihypertensive therapy is required in case of stroke and

Heart failure
Aortic dissection
Acute myocardial infarction
Acute renal failure
Thrombolysis or i.v. heparin

The only exceptions to this advice are concomitant heart failure, aortic dissection, acute myocardial infarction (AMI; although extreme lowering of BP is negative for myocardial infarction (MI) patients as well) or acute renal failure, which are themselves hypertensive emergencies and need more aggressive treatment of BP. In the case of thrombolytic or anticoagulant treatment stricter but cautious BP control is necessary.

Recommended target BP in patients
Recommended drugs for BP treatment
Avoid nifedipine and in general abrupt BP decrease
Avoid and treat hypotension particularly in unstable patients with adequate hydration and, when required, volume expanders and/or catecolamines (epinephrine 0.1-2 mg/h plus dobutamine 5-50 mg/h)


1.	If DBP > 140 mm Hg in two measurements 5 minutes apart: i.v. infusion of nytroglycerine or sodium nitroprusside (0.5-1.0 mg/kg/min) (monitoring the risk of brain oedema particularly in large infarcts)
2.	If SBP> 220 mm Hg, or DBP 120-140 mm Hg, or mean BP > 130 mm Hg in two measurements 20 minutes apart, give labetalol 10 mg i.v. in 1-2 minutes; the dose may be repeated or doubled every 10-20 minutes up to a total dose of 300 mg. Then labetalol can be administered every 6-8 hours if necessary. Contraindications to labetalol: asthma, heart failure, severe arrhytmias
3.	If SBP 185-220 mm Hg or DBP 105-120 mm Hg, avoid treatment unless there is cardiac failure, aortic dissection, AMI.
4.	Avoid administering sublingual calcium antagonists
5.	In case of brain haemorrhage the thresholds for treatment are SBP > 180 or DBP> 105 mm Hg
6.	Monitor the neurological status during treatment to avoid deterioration
7.	Although threshold BP values to define hypotension have not been determined, in patients with dehydration or with blood pressure values that are significantly lower than is usual for the patient, the use of fluids or, in case of heart failure, the use of dopamine in the treatment is recommended

References:
EUSI Recommendations. 2002, www.eusi-stroke.com
Adams et al. Stroke 1994; 25 (9): 1901-1914
American Academy of Neurology. 2000, www.aan.com

Fluids / Electrolyte balance

Avoid an excessively positive balance to avoid
Maintain a 300-350 ml negative fluid balance in patients with brain oedema
Hypotonic solutions (sodium chloride 0.45 % or glucose 5.0 %) are contraindicated: risk of brain oedema increase
Glucose solutions are contraindicated: detrimental effects of hyperglycaemia

Reference:
EUSI Recommendations. 2002, www.eusi-stroke.com

Glucose Metabolism

Hypoglycaemia may be present in malnourished stroke patients
Monitoring of serum glucose levels is required particularly in known diabetic patients
Treatment of serum glucose levels > 10 mmol/l with insulin titration
Glucose solutions are contraindicated due to the detrimental effects of hyperglycaemia (see also above)
Immediate correction of hypoglycaemia is required with the addition of 100 mg thiamine in malnourished or alcohol-addicted patients

Accurate monitoring of serum glucose levels is necessary whenever high serum glucose levels are found at hospital admission, particularly in known diabetic patients. A blood glucose level equal to or above 200 mg/dl or 10 mmol/l requires immediate insulin titration. Unless the blood glucose level is known, no glucose solution should be given to a stroke patient. A pilot study on patients with mild to moderate hyperglycaemia (plasma glucose between 7.0 and 17.0 mmol/l) randomized to receive either a 24-hour infusion of 0.9% (154 mmol/l) saline or a 10% glucose potassium insulin (GKI) infusion at 100 ml/h, showed that GKI was safe, producing a physiological but attenuated glucose r esponse to acute stroke. A randomized controlled trial is ongoing.

Hypoglycaemia, which may be present in malnourished stroke patients should be treated by i.v. dextrose bolus or by infusion of 10-20 % glucose, preferably via a central venous line, with the addition of 100 g of thiamine in malnourished or alcohol-addicted patients.

References:
Scott et al. Stroke 1999; 30 (4): 793-799.
GIST-Investigatoers. Stroke 2002; 33 (1): 654.

Body Temperature

Results from small randomized trials with high-dose antipyretics are controversial
Treatment of body temperature ≥ 37.5 °C is advisable
Infections are a risk factor for stroke and in up to 85 % of cases fever is due to an infection after stroke
In case of fever it is necessary to determine the site and nature of any possible infection in order to start tailored antibiotic treatment
Antibiotic, antimycotic or antiviral prophylaxis is not recommended in immunocompetent patients

References:
Kasner et al. Stroke 2002; 33 (1): 130-134.
Grau et al. Stroke 1995; 26 (3): 373-379.
Georgilis et al. J Intern Med 1999; 246 (2): 203-209.

Dysphagia

Dysphagia is

Present in up to 50% of patients
Predictor of poor prognosis
Risk for aspiration and pneumonia
Malnutrition
Dehydration with plasma volume contraction

Malnutrition may be favoured by dysphagia which is present in up to 50% of stroke patients, and not only those with brainstem infarcts but also in case of hemispheric stroke. Dysphagia is also responsible for a risk of aspiration and pneumonia, and of dehydration with plasma volume contraction.

Dysphagia should be tested in all acute stroke patients at hospital admission. The test should be repeated every other day when the baseline evaluation is abnormal, and dietary texture, bolus size and feeding posture should be controlled. In cases of severe dysphagia, enteral nutrition is usually recommended, while the parenteral route should be adopted only when enteral nutrition is not feasible, or as a supplement when enteral nutrition is not sufficient. Whether to use a nasogastric tube or transluminal percutaneous gastrostomy and when starting feeding are still the subjects of research.

References:
Mann et al. Cerebrovasc Dis 2000; 10 (5): 380-386.
Smith et al. Age Ageing 2000; 29 (6): 495-499.
Smithard et al. Stroke 1996; 27 (7): 1200-1204.

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