Box 33 Suggested guidelines for the use of intravenous rTPA in ischaemic stroke108

Intravenous r-TPA should be considered in all patients with a proven ischaemic stroke presenting within three hours of onset.

Recommended dose is 0-9 mg/kg, up to a maximum of 90 mg, the first 10% as a bolus, the rest as an infusion over 60 minutes.

Thrombolysis should be avoided in cases where the CT suggests early changes of major infarction (for example, sulcal effacement, mass effect, or oedema).

Thrombolytic therapy should only be administered by physicians with expertise in stroke medicine, who have access to a suitable stroke service, with facilities for identifying and managing haemorrhagic complications.

Exclusion criteria: use of oral anticoagulants or INR greater than 1-7; use of heparin in preceding 48 hours or prolonged partial thromboplastin time; platelet count less than 100 000/mm3; stroke or serious head injury in the previous three months; major surgery within previous 14 days; pretreatment systolic BP greater than 185 mmHg or diastolic greater than 110 mmHg; rapidly improving neurological condition; mild isolated neurological deficits; previous intracranial haemorrhage; blood glucose greater than 22 mmol/L (400 mg/dl) or less than 2-8 mmol/L (50 mg/dl); seizure at stroke onset; gastrointestinal or urinary bleeding within previous 21 days; or recent myocardial infarction.

Caution is advised before giving r-TPA to patients with severe stroke (NIH Stroke Scale Score greater than 22).

It is recommended that treatment and adverse effects are discussed with patient and family prior to treatment.

The individual threshold for using early anticoagulation is very variable and some physicians use anticoagulants for specific situations such as basilar artery thrombosis or intracardiac thrombus.

Although we know that oral anticoagulation with warfarin is effective in the secondary prevention of stroke in patients with atrial fibrillation,93,94 we have considerable difficulty deciding when to start warfarin after the primary event. We tend to delay longer (perhaps by two weeks) in patients with large ischaemic cerebral lesions, believing that they are more likely to suffer ill effects (mainly haemorrhagic transformation) from anticoagulation, although this is not evidence based. The question of whether to anticoagulate patients with other potential cardioembolic sources, such as


Expt n/N

Ctrl n/N

Peto OR Weight Peto OR (95%CI fixed) % (95%CI fixed)

Unfractionated heparin (subcutaneous) vs control

1ST 1997 6063/9717

Subtotal (95%CI) 6063/9717

Chi-square 0 00 (df = 0) Z = 0-02 Low-molecular-weight heparin vs control FISS 1995 100/207

FISS-bis 1998 300/250

Subtotal (95%CI) 400/723

Chi-square 6-24 (df=1)Z= 1-20 Heparinoid (subcutaneous) vs control

CAZZATO 1989 13/28

Subtotal (95%CI) 13/28

Chi-square 0 00 (df = 0) Z = 0-40 Heparinoid (subcutaneous) vs control

TOAST 1998 159/641

Subtotal (95%CI) 159/641

Chi-square 0 00 (df = 0) Z = 0-61 Total (95%CI) 6635/11109

6062/9718 6062/9718

68/105 142/250 210/355

15/29 15/29

167/635 167/635


12 1 5 10 Favours treatment Favours control

Figure 3.2 Results of a systematic review of the randomised trials of anticoagulants in acute presumed ischaemic stroke. There was no significant effect of anticoagulant treatment on death or dependency at the end of follow up (greater than one month)

mitral valve disease without AF, is very difficult, with little evidence to guide the physician.

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