|
|
|
|
 |
|
The term 'general treatment' in acute stroke care refers to treatment strategies
aimed at stabilising the critically ill patient, in order to control systemic problems that may negatively influence
stroke outcome and to provide an optimum physiological basis upon which specific therapeutic strategies may be applied.
General management of stroke patients includes respiratory and cardiac care, fluid and metabolic management, BP control,
and perhaps treatment of elevated intra-cranial pressure. In addition, treatment of seizures and prophylactic measures
concerning DVT, pulmonary embolism, dysphagia, aspiration pneumonia, other infections, and decubital ulcer are part
of the general treatment of the patients. In all stroke patients neurological status and vital functions should be
continuously or intermittently monitored. The neurological status is best monitored using validated neurological
scales, such as NIH Stroke Scale, the Scandinavian Stroke Scale, the Glasgow Coma Scale and others.
The role of antithrombotic therapy in acute stroke is to prevent recurrent strokes and further vascular events.
Administration of heparin or low-molecular-weight heparin, in bedridden patients after stroke, is recommended only to
reduce the number of DVTs and subsequent pulmonary embolism (PE) and only after 24 hours following thrombolysis.
However, there is a risk of intracranial bleeding. Acute treatment with ASA can be started acutely or, following
thrombolysis, 24 hours later. Studies in Cologne have suggested that in patients already receiving ASA treatment,
intracranial bleeding is more likely associated with thrombolysis given later than 3 hours following acute stroke.
Caution is required.
The aim of neuroprotection is to sustain neuronal survival in the presence of ischaemia, until perfusion can be
restored spontaneously or through natural reperfusion and collateral circulation. This could be achieved by
interrupting the ischaemic cascade or by assisting resistance to ischaemia. Even temporary protection may be
enough to extend the time window during which thrombolysis may safely be administered.
Although thrombolysis is already administered as rapidly as possible, delays still occur whilst imaging is performed
and reperfusion does not necessarily take place until an hour or two after thrombolysis is commenced. A neuroprotective
agent that is safe for use in haemorrhagic stroke may be able to be administered immediately on recognition of stroke,
and may protect the brain until reperfusion occurs.
Up to 85 % of all strokes are of ischaemic origin and mostly due to blockage of a cerebral artery by a blood clot. After
introduction of thrombolytic therapy for the treatment of acute myocardial infarction in the early 1990s, major trials
for the evaluation of this new therapeutic approach in ischaemic stroke were initiated. A good overview of thrombolytic
therapy treatments is given in the textbook by Fiebach & Schellinger. The first anecdotal report of thrombolytic therapy
for ischaemic stroke dates back to the early 1960s. Three trials in the beginning of the 1980s investigated the effect
of low-dose intravenous urokinase for the therapy of acute ischaemic stroke. The three dose finding studies in the
1980s differ from others in several ways, such as the late timepoint of inclusion (up to 5 or 14 days after stroke
onset, respectively), the exclusion of presumed cardioembolic stroke, application of low doses of urokinase given
daily for a period of several days, and the lack of assessment of clinical outcome expect death and ICH. In the
early 1990s three small trials of intravenous thrombolysis with rt-PA were done, two of them in Japan. Although not
large enough to prove the efficacy, they clearly showed the feasibility of early thrombolytic therapy and also
suggested a reasonable degree of safety and a potential benefit. From 1995 onwards large blinded or double-blinded,
randomized, and placebo-controlled trials with rt-PA and streptokinase were done.
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.
Toni et al. Arch Neurol 1995; 52 (7): 670-675.
EUSI Recommendations. 2002, www.eusi-stroke.com
Grotta JC. Stroke 2002; 33 (1): 306-307.
Lees KR. Stroke 2002; 33 (1): 308-309.
Schellinger PD, Hacke W. In Fiebach JB, Schellinger PD 2003; 11: 63-74. |
|
 |
|
© 2005 Boehringer Ingelheim GmbH, Germany. All rights reserved.
|
|
|
|
|
|
