Acute Stroke – Managing Acute Stroke

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Current Therapy Acute Stroke

Once a firm diagnosis is made, specific therapy and care begin. Some traditional treatments are known to have uncertain foundation. Active research is being directed to the causes of neuronal damage, the progression of acute stroke and alleviation of the insult.

Stroke may be categorized as either ischaemic or haemorrhagic in nature. While ischaemic cerebrovascular disease predominates throughout the world, cerebral haemorrhage may account for 30 to 40% of stroke among Chinese and Japanese. As cerebral haemorrhage patients may be fully alert and clinically resemble those suffering from ischaemic vascular disease, treatment of stroke must be based on firm radiological identification of the underlying pathology. The cause of stroke has to be clearly identified so that specific risk factors are controlled, and treatment is tailored to individual requirements.

General Management of Acute Stroke

Good management of stroke patient should begin with sound basic diagnosis, investigation and nursing care. Dedicated strict medical and nursing care in acute stroke units has been shown to reduce functional disabilities and the need to long-term hospitalization, even when drug therapy is identical to that given in general medical units. The difference in outcome seems attributable simply to greater care in diagnosis, therapy, and overall management of preventable complications. Adequate nutrition, fluid and electrolyte balance should ensured; nasogastric feeding may be necessary in those who cannot be fed.

Stuperouos or comatose patients may need airway protection to prevent aspiration, frequent suction as well as semi-Fowler positioning. The Tredelenberg position is indicated in the case of proporsional cerebral ischaemia. Prolonged bed confinement leads to complications such as infection, thrombophlebitis, pulmonary embolism and decubitus ulcers. The immobilized patient should be turned at least 2-hourly to prevent ischaemic necrosis of skin and development of bed sores, as well as infection. More frequent positional changes are likely to be beneficial since kinetic therapy using a rotating bed which turns patients 8 rotations/hour has been reported to reduce even further the frequency of infection. Joint contractures can be prevented by physical therapy, while anterior dislocation of the humeral head can be prevented with good positioning and the use of slings. Rehabilitation should start as early as possible.


Fever in a patient with ischaemic stroke is usually secondary in infection, most commonly aspiration or infectious pneumonia. Pulmonary atelectasis may be prevented by periodic hyperventilation and forceful coughing. Chest movement on hemiplegic side tends to be decreased so attention should be paid to that side. Pneumonia is a major cause of death in stroke patients, and raised respiratory rate and development of fever can aid early recognition of this complication. Urinary tract infection is also common because of the frequent use of indwelling catheters, as well as inability to empty the bladder fully with resultant urine statis in those without catheter. Venous thrombosis in the paralysed leg maybe prevented by the use of the leg wrappings, passive leg movements, adequate hydration and the use of low dose subcutaneous heparin. This complication, however, is uncommon among Chinese so that only selective use of anticoagulation is necessary in this population. Particular care should be taken in brainstem stroke as aspiration and cardio-respiratory complications including sleep apnoea are common.


Hypertension is a major risk factor for stroke, and is therefore frequently found on admission. However, many patients will have spontaneous reduction of the hypertension in a few days. In deciding how soon a raised blood pressure should be brought down to normal levels after a stroke, it is worth considering that when autoregulation is impaired during acute ischaemic stroke and the cerebral blood flow becomes passively dependent on arterial pressure, the marginal ischaemic penumbra may suffer reduction in blood flow with reduction of the blood pressure. Furthermore, decrease in blood pressure may reduce flow and therefore enhance thrombus formation.

In case of cerebral haemorrhage, however, a higher blood pressure may be necessary to provide adequate cerebral perfusion pressure in the presence of a raised intracranial pressure. For the above reasons, aggressive treatment of hypertension in the acute phase may be both unnecessary and dangerous. It is prudent to aim for stabilization at a lower level rather than a normal level, and reduce blood pressure gradually unless there is extreme hypertension, hypertensive encephalopathy, myocardia ischaemia aggravated by the hypertension, or aortic dissection. Furthermore, drugs such as nitroprusside, hydralazine, clonidine, diazoxide which reduce cerebral perfusion, should be either avoided or used with great caution.

Experimental studies have shown that hyperglycaemia intensifies ischaemic cerebral injury. There is also evidence that stroke patients with higher glucose levels do less well. While controversy exists as to whether this represents a deleterious effect of hyperglycaemia or inversely the stress effect of a large infarct on glucose homeostatis, the observation does point to the necessity of monitoring glucose levels in patients with stroke and a more judicious use of glucose infusions.


Steroids are frequently prescribed for cerebral oedema in stroke. However, unlike the extracellular vasogenic oedema that follows ischaemia does not respond to steroid therapy. A controlled study failed to show that high dose steroids given to patients with cerebral infarction have any beneficial effect. In addition, complications of infections were more common with steroids. Mannitol and other dehydrating agents, although having fewer side effects, have been equally ineffective. surgery, however, may be useful in cases of severe ischaemic cerebellar swelling causing brainstem compression.


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