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Neurology India
Medknow Publications on behalf of the Neurological Society of India
ISSN: 0028-3886 EISSN: 1998-4022
Vol. 50, Num. s1, 2002, pp. S37-S49

Neurology India, Vol. 50, (Suppl. 1), Dec, 2002, pp. S37-S49

Critical Care Management of Acute Stroke

A.K. Meena, A. Suvarna, S. Kaul

Department of Neurology, Nizam's Institute of Medical Sciences, Hyderabad - 500 082, India.
Correspondence to : Dr. A.K. Meena, Department of Neurology, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad - 500 082, India.

Code Number: ni02161


Treatment of acute stroke in an intensive care unit improves the outcome by reducing the mortality and morbidity. In addition to the primary neurological condition that affects the outcome, the secondary complications and associated co-morbid conditions also influence the outcome. It is essential to monitor and maintain the general physiological conditions in the neurologically sick patients. Maintenance of a clear airway is important to prevent hypoxic insult to the brain in stroke patients whose airway is compromised. Mean arterial blood pressure should be maintained > 110mm of Hg. The choice of antihypertensive is labetolol. Drugs causing raised intracranial pressure (ICP) should be generally avoided. Cardiac arrhythmias should be monitored and treated. Treatment of ICP by osmotic agents is the usual practice. Hyperventilation is reserved for patients who are coning and is only a temporizing measure prior to surgery. Hemicraniectomy in malignant middle cerebral artery territory infarcts reduces the mortality significantly. Insulin therapy may be required to maintain a normoglycemic state for preserving the functionally impaired neurons. Infections should be treated by appropriate antibiotics. Care should be taken to prevent aspiration, and deep vein thrombosis. Intravenous thrombolysis for the eligible candidates and Aspirin for the rest is the recommended therapy for acute ischemic stroke.

Key words : Acute stroke, Intensive care, Hypertension, ICP.


Intensive treatment of stroke especially in stroke units or intensive care units (ICU) definitely improves outcome and lowers mortality after stroke.1 There are three main areas in the treatment of acute stroke. i) Treatment of general physiological conditions that need to be optimized in the setting of acute stroke. ii) Prophylactic treatment of potential complications which may be either neurological or medical. iii) Specific therapy directed against different aspects of stroke pathogenesis which include treatment for recanalization and neuroprotection.

Although most stroke patients can be cared for in a general neurology ward, it becomes important to recognize when patients with stroke are in need of more specialized monitoring. Indications for admission to intensive care units or stroke unit include requirement for airway management, hemodynamic monitoring, treatment for increased intracranial pressure (ICP), observation for neurological deterioration and patients receiving thrombolytic therapy.

Airway management

Stroke patients may require intubation for either airway obstruction or acute respiratory failure. Airway obstruction develops due to three reasons. First, in acute stroke patients with decreased level of sensorium the tongue falls backward, intermittently obstructing the airway, due to lack of tone in the tongue and pharyngeal muscles. Second, in patients with brainstem stroke, the gag and cough reflex is reduced. In addition patients may be unable to clear the secretions.2 The criteria for intubation and extubation are given in table I.3 Stroke patients may develop respiratory failure from aspiration or community acquired pneumonia.

Initial management of intermittent airway include, placement of oral or nasal airway to prevent obstruction and allow easier access for suctioning. Frequent assessments are necessary to check for sonorous respiration, presence of rhonchi, increased respiratory rate, decreased oxygen saturation, or increasing suctioning requirements. Any of these should alert the physicians to a worsening respiratory status. Use of mechanical ventilation in a patient with reduced level of consciousness due to large infarcts remains controversial. Mortality of 51-90% has been reported in patients receiving mechanical ventilation.4-7 These patients are usually intubated to secure airway and to institute therapies such as hyperventilation. Very few patients with ischemic stroke require intubation (6-8%) and those who do, have a poor prognosis.7,9 Independent predictors of death in patients requiring ventilators include, age, poor Glasgow coma scale(GCS) score and respiratory failure.10 Patients with brainstem stroke who require ventilator have very poor outcome.10

At the time of intubation, the use of medication, that provide adequate muscle relaxation, without leading to haemodynamic instability and prevent elevated ICP from tracheal stimulation) is recommended.3,11 If anesthesia is used for intubation, thiopental (3-5 mg/kg IV) can be used in hemodynamically stable patients whereas, etomide is an ideal drug, in a hemodynamically unstable patient, but it is short acting (0.3-0.5m/kg/IV). Propofol (2-2.5mg/kg IV) can be used but it causes seizures and hypotension.12,13 Muscle paralysis is usually avoided, as frequent neurological examination cannot be performed. In patients with increased ICP, neuromuscular blockade should be induced with vecuronium.14 Succinylcholine is usually avoided as it increases ICP and causes hyperkalemia in patients with neuromuscular disease. Despite all efforts to avoid hemodynamic compromise during intubation, hypotension may result especially in aged patients.

Modes of mechanical ventilation : Oral intubation is the safest method of intubation in patients with stroke.15 The choice of ventilation is usually based on the reasons for intubation, either neurological (airway protection) or primary respiratory failure. In the former case, pressure support ventilation is the used. The amount of additional pressure is adjusted to achieve a total volume of 5-8ml/kg and a respiratory rate <25 breaths/minute. Patients with coma or patients with an abnormal respiratory pattern, need controlled mechanical ventilation.16 Synchronised intermittent mandatory ventilation (SIMV) is the preferred method of ventilation. Positive end expiratory pressure (PEEP) during ventilation should be avoided in patients with significantly increased ICP although setting up to 10cm H2O can be tolerated.17,18 Patients with impaired oxygenation (Pneumonia, ARDS, neurogenic pulmonary edema) require complicated mode of ventilation such as pressure control, inverse ratio ventilation, high level of PEEP and inhaled nitrous oxide, If no improvement is seen within 7-10 days, tracheostomy should be instituted as early as possible.

Hemodynamic monitoring

Management of haemodynamics in patients with cerebrovascular disease is complex. Cardiovascular abnormalities (arrhythmia and blood pressure) are often responsible for acute neurological illness, such as stroke and vice versa. Because the risk factors are shared, patients with cerebrovascular diseases are also at high risk for cardiac ischemia. Most haemodynamic manipulation in the neurological intensive care unit involves : i) management of hypertension in the setting of an acute neurological insult ii) management of cardiac arrhythmia and functional cardiac disturbances concurrent with or caused by acute neurological insults iii) treatment of vasospasm following subarachnoid haemorrhage

Management of hypertension : Blood pressure (BP) management is a critical and controversial issue and depends on the clinical circumstances.19-24 Hypertension (HTN) is a well-known risk factor for stroke and 70-80% of patients with acute stroke have high blood pressure at admission25-27 and BP spontaneously normalizes over a few hours to 7-10 days.26-28 Continuous BP monitoring should be done to avoid the 'white coat effect'.29, 30 In animal studies it has been shown that high BP increased the risk of hemorrhagic transformation. However the data in human is inconclusive.31-32 Although uncontrolled HTN might worsen the cerebral edema and outcome may be poor, experimental data regarding this has been inconsistent.33 Very few studies in humans have shown that treatment of HTN within 24 hours definitely reduced cerebral edema and improved outcome in ischemic stroke patients.34 In fact, review of the available data in humans has not shown any convincing link between hypertension at admission and morbidity and mortality.35-37 Aggressive treatment of BP in chronically hypertensive patients might in fact reduce the cerebral blood flow (CBF) and worsen the ischemic damage and neurodeficit,37 as cerebral auto regulation is often set at a higher pressure in chronic hypertensives , and may actually be impaired in older people and in patients with ischemic stroke.38-40 Neurons in the penumbral region which are functionally impaired but still viable, are vulnerable to the reduction in BP in the face of reduced blood supply.41 In patients with ischemic stroke who have high grade vascular stenosis, lowering of BP might increase the ischemia and facilitate complete occlusion of vessels.24 Anecdotal case reports and recent studies have shown that lowering of BP was associated with worse outcome.42,43 SPECT studies on patients randomized to nicardipine within 72 hours had shown a decrease in CBF associated with drop in BP.44

Recommendations for blood pressure management : As there are no controlled studies addressing the impact of HTN treatment on outcome in ischemic stroke, recommendations are largely empirical. The American Heart Association, suggests that blood pressure in acute stroke should not be treated unless patients have severe HTN (mean arterial pressure >130mm or systolic BP > 220 mm of Hg).45 Occasionally, other serious diseases mandate aggressive lowering of blood pressure in people with ischemic stroke. These include acute myocardial infarction, acute renal failure and dissection of aorta.23 For patients receiving rt-PA, guidelines recommend stricter BP control at a systolic pressure of 185 mmHg and diastolic pressure of 110 mmHg.46

Choice of antihypertensive drug : The most ideal antihypertensive drug in ICU setting would be the one with a short half-life, moderate efficacy and devoid of side effects like sedation. It should not reduce CBF or ICP. Characteristics of various drugs used in the treatment of hypertension in acute stroke are summarized in table II and III. Labetolol, a combined a and b blocker is the ideal drug of choice. Angiotensin converting enzyme inhibitors are preferred because they do not have any effect on ICP and CBF.47,48 Calcium channel blockers may increase the ICP but they maintain or increase CBF. When indicated, we preferably use intravenous labetolol, or ACE inhibitors in our Intensive Care and Stroke unit. Conventional drugs, which act as primary vasodilators such as nitroglycerine, sodium nitroprusside and hydralazine, can increase ICP and should be used with caution.

Hemodynamic augmentation

Experimental models of ischemic stroke have shown that induced hypertension can decrease the infarct size by increasing the CBF. Studies in humans have shown that vasopressor use in stroke patients improved the outcome and it was safer.49,50 However this form of therapy needs further evaluation.

ECG changes, cardiac arrhythmias and myocardial damage

More than 85% of patients with stroke have abnormal ECGs. New onset ECG changes have been reported to occur in about 15-30% of ischemic and hemorrhagic strokes.51,52 These include QT prolongation, U waves, T wave abnormalities and ST segment elevation or depression. The exact nature of these ECG changes is unclear. In many cases the changes are transient and may be due to stroke itself. However, many patients have concomitant cardiovascular disease; 30-65% of patients with stroke have asymptomatic coronary artery disease.53 In one study 15% of patients with stroke were found to have a coincident myocardial infarction based on ECG criteria.51 However, accurate data to support this incidence of true myocardial damage is scanty. Elevated CK - MB levels have been found in 11% of patients, however, these levels rise slowly and peak 4 days after the event unlike true myocardial infarction.54 These changes are thought to be due to increased sympathetic activity and are reported more frequently with left insular damage.55 There is one case report of "stunned myocardium" in stroke similar to that seen in subarachnoid hemorrhage.56 Stroke patients have a 25-39% incidence of arrhythmias on admission ECG, the most common of which is atrial fibrillation. Holter studies, however, show a higher incidence of arrhythmias.57,58 Patients with recent onset ECG changes have a higher mortality, especially those with ventricular arrhythmias. Despite this, the value of routine ambulatory Holter monitoring in patients with stroke has been questioned because it does not usually lead to a significant alteration in management.59

Elevated ICP and brain edema

Ischemic brain edema occurs during the first 24-48 hours after ischemic infarcts. In younger patients with complete middle cerebral artery (MCA) infarction, brain edema and elevated ICP may become a major complication and may lead to herniation and death.60 These patients usually show a rapid decline in consciousness and develop the signs of herniation 2-4 days after the onset of symptoms. Outcome was fatal in the majority of these patients, with a mortality of about 80% with standard treatment.60,61 Appropriate treatment of raised ICP in large infarcts depends on the knowledge of ICP and the simplest way is to measure the ICP by intraparenchymal fiberoptic pressure monitor. However in patients with large hemispheric infarcts, the neurologic examination is more sensitive than the transduced ICP for predicting outcome.62,63 The insensitivity of ICP monitoring in ischemic stroke is most likely related to the fact that transtentorial herniation occurs because of local tissue shifts, which are seen before a global rise in ICP.50

General care of patients with raised ICP

Patient Positioning : Cerebral perfusion pressure is optimized when the head of the bed is at 15-30o above the horizontal.64-66 Because head turning can impair jugular venous return, patients should be kept supine with the head positioned straight ahead.

Intubation : The anesthesiologist should always be apprised of patients with increased or potentially increased ICP as this may change their intubation protocol. For instance, succinylcholine can increase ICP,67 while standard rapid induction techniques may decrease MCA blood 'flow'. In general, induction of anesthesia should be done with an agent that may have neuroprotective and ICP lowering effects, such as midazolam, etomidate or thiopental. The cough reflex, which can increase ICP, should be suppressed with lidocaine and neuromuscular blockade achieved with a non-depolarizing agent like rocuronium or vecuronium. Aggressive suctioning and neck procedures should be done with caution.

Fluid management : Raised ICP was historically managed by fluid restriction in an effort to avoid increasing brain water. It was later discovered that hypovolemia could rapidly lead to decrease in cerebral perfusion pressure (CPP) and thus increasing the hypoxic-ischaemic injury. Also there is no evidence that fluid restriction improves brain edema.67 Free water should be avoided and isotonic fluids should be given. Normal serum osmolality should be maintained. Patients should be kept euvolemic at all times. Hypertension and hyperthermia should be treated appropriately as both fever and high BP increase cerebral edema.

Treatment for increased ICP

Various modes of treatment available for management of raised ICP are summarized in table IV and are as follows.

Mannitol : Osmotherapy is usually accomplished with mannitol, which has an osmolality of 5.5 mOsm/kg. In addition to its osmotic effects, mannitol decreases blood viscosity and causes vasoconstriction. Complications of therapy include hypovolemia, decreased CPP, hyperkalemia, renal failure, and rebound edema.69 The other osmotic agents are glycerol and urea, the clinical effects of which are unproven.

Hypertonic saline
Clinical studies show that hypertonic fluids can effectively reduce ICP when standard therapies have failed.70-72 An increase in serum sodium concentrations to 145 to 155 mmol/L will reduce the mean ICP and decrease lateral displacement of the brain in patients with head trauma and postoperative edema.73 In patients with large hemispheric infarcts, treatment with hypertonic saline in hetastarch was found more effective in treating elevated ICP than mannitol.74 Complications of hypertonic saline therapy include diabetes insipidus, pulmonary edema, congestive heart failure, rebound edema and theoretically, increased mid-line shift.

Hyperventilation Hyperventilation decreases ICP because it causes vasoconstriction of the cerebral vessels and thereby decreases cerebral blood volume (CBV).75 Since hyperventilation causes vasoconstriction, it can exacerbate cerebral ischemia.76 Hyperventilation is the most effective treatment of acute herniation, but the efficacy of hyperventilation wanes quickly.77 Chronic hyperventilation also has been associated with worse outcome in clinical studies.78 Hyperventilation is most effective when CBF is hyperemic and should be done with SjvO2 (jugular vein O2 saturation) or AVDO2 (arterio-venous difference of O2) monitoring.79 Hyperventilation is best achieved by increasing the ventilatory rate to 16- 20/sec. The peak effect is achieved within 30 minutes. Once ICP is stabilized, hyperventilation should be tapered gradually over 6-12 hours to prevent rebound increase in ICP.

High dose Barbiturates
Barbiturates are often used to treat patients with refractory increase in ICP. Barbiturates decrease the CBF thereby reducing the CBV and ICP.80 Early experimental studies in stroke suggested that barbiturates may improve outcome, but a systematic review of these studies suggest that the benefit was primarily related to hypothermia.81 In a recent observational study in patients with large hemispheric infarcts barbiturate therapy did not improve clinical outcome.63 Its clinical utility is limited by systemic side effects, including hypotension and cardiac depression, and requires EEG monitoring. Use of barbiturate coma in stroke is not recommended based on the existing data.

Induced hypothermia
Small increases in core temperature can lead to significant increase in CMRO2.83 Induced hypothermia can be used to treat refractory elevations in ICP. During hypothermia CMRO2 is reduced there by decreasing the CBV and ICP.84 Hypothermia is found to be neuro-protective in experimental stroke models. Recently Schwab et al showed that hypothermia reduces mortality in large hemispheric strokes. It is also found to be of benefit in head injury patients.85

Hemodilution therapy has been popularly used in stroke treatment especially in European countries. There are experimental evidences that moderate isovolemic hemodilution increase CBF and decrease infarct volume,86,87 but in prospectively randomized controlled trials hemodilution failed to improve clinical outcome.88,89

De-compressive surgery
Malignant MCA Infarction : The rationale of decompressive surgery is to allow expansion of the edematous tissue away from the lateral ventricle, the diencephalon and the mesencephalon, to reduce ICP, to increase perfusion pressure and to preserve CBF by preventing further compression of the collateral vessels. These factors may help to increase CBF in areas surrounding ischemic regions, thereby preventing further brain tissue necrosis. In large prospective uncontrolled case series, surgical decompressive therapy in hemispheric spaceoccupying infarction lowers mortality from roughly 80% down to 40% without increasing the rate of severely disabled survivors.61 Early decompressive surgery (e.g. within the first 24 h after stroke onset) can reduce mortality even more pronouncedly.90 A prospective, multicentre study protocol has been recently developed and is now underway.

Cerebellar Infarction : Decompressive surgery is widely considered the treatment of choice for a spaceoccupying cerebellar infarction, although the scientific basis for this is by no means any more solid than in hemispheric infarction. Comatose patients with space-occupying cerebellar infarctions have a mortality of about 80% if treated conservatively. This high mortality can be lowered down to 30% if decompressive surgery is performed.91,92 Like in space-occupying supratentorial infarction, the operation should be performed before signs of herniation are present. The prognosis among survivors is very good, even if they were comatose when the operation was performed. Most of them regain a Barthel Index of 85 or higher. It should be noted, however, that these are the results of open, small or medium-sized case series, one of them prospective, but mostly retrospective. Data from controlled, randomized trials are lacking.

Temperature control
Fever is very common in neurointensive care units (NICU) affecting 30-60% of patients with ischemic stroke and intracerebral hemorrhage,93 SAH94 and head injury. Hyperthermia is a proven factor for cerebral injury in experimental models of focal and global cerebral ischemia95-97 and its harmful effect persists even if it appears days after the start of ischemia.98,99 The association between hyperthermia, early neurological deterioration, increased morbidity and mortality has also been documented in patients with acute stroke.100 Hyperthermia causes neuronal injury by several mechanisms.

The cause of post-stroke fever is unclear but in acute stages it is generally related to the stroke itself, CNS inflammation or due to the production of endogenous pyrogens. Fever in the later phases of stroke is usually due to infectious causes. Although it is generally accepted that fever should be reduced by aggressive measures the most effective method remains unclear. Two types of interventions can be used to reduce increased body temperature: Antipyretics (Acetoaminophen, aspirin and NSAIDS) and external cooling. Antipyretics act by lowering the hypothalamic set point which is increased in fever.101 Antipyretics are not effective in fever due to an impaired thermoregulatory mechanism. In such instances achieving a core temperature of 30oC requires invasive measures and has potential life threatening complications. Presently the most recommended method of external body cooling is aircirculating blankets, which is minimally invasive.102 Other methods of surface cooling is by ice packs, fans, water cooled blankets. Fever due to infectious causes responds to antipyretics combined with aggressive treatment with appropriate antibiotics.

Glucose metabolism
Both hyperglycemia and hypoglycemia can contribute to worsening of neuronal injury in acute ischemic stroke through several mechanisms.103-105 Experimental studies suggest that insulin-induced normoglycemia may improve stroke outcome.105 Hence monitoring of glucose level in diabetic stroke patients especially patients on steroids becomes an important task in intensive care units.106 Aggressive attempts to normalize blood glucose levels are recommended especially because combination of insulin and glucose improves substrate delivery to ischemic tissue.107 A target blood glucose level of <200mg/dl is achieved by administering insulin by sliding scale coverage. If it fails a continuous infusion may be necessary.

Brain injured patients are hypermetabolic and hypercatabolic. Therefore, adequate nutritional support is important for their recovery.108,109 If a patient is unable to eat safely, enteral feeding should be initiated as soon as possible via a nasogastric tube. Gastric feeding, although the commonest route often, results in inadequate nutritional support due to delayed gastric emptying. The ideal enteral formula should contain adequate caloric intake (25 to 30 Kcal/Kg/day) and avoid hypo-osmolarity and hyperglycemia.109 To prevent reflux and aspiration during tube feeding, elevating the head of the bed, monitoring gastric residuals and administering metoclopramide (10mg per tube every 6 hours) are usually effective. Some patients with persistent delayed gastric emptying will need feedings into the small bowel. Jejunal feeding is well tolerated and it enables early, within 72 hours, a high caloric intake and better nitrogen balance while preventing regurgitation and aspiration.110 Tube feedings along with sucralfate or histamine-2 blockers are used to prevent stress ulcers.111,112 Care must be taken to avoid giving sucralfate at the same time as phenytoin because it will interfere with phenytoin absorption.

Agitation is common in acute stroke.113 Oxygen consumption is increased in such patients. Short acting or easily reversible analgesic and anxiolytic should be used so that clinical examination can be performed. Propofol is the preferred drug of choice.114 However short acting benzodiazepins like midazolam can also be used.115 These drugs do not affect ICP, CPP, and CMRO2. Propofol actually reduces ICP and CMRO2.116

Deep venous thrombosis (DVT) prophylaxis
An autopsy series of 101 patients with neurologic disorders found a 24.8% incidence of pulmonary embolism (PE).117 Stroke patients are at high risk for DVT and subsequent PE due to their immobility and advanced age. Pneumatic compression boots decrease the incidence of DVTs but not PE in neurosurgical patients,118 and should be used on all patients until they are mobile. The combination of pneumatic compression boots and low-dose heparin may decrease the incidence of PE.119 Therefore, patients at low risk of hemorrhagic complications, such as those with ischemic stroke, should also be administered low dose heparin (5000u SC bid). Neurologic contraindications for subcutaneous heparin include intracranial hemorrhage (relative), unprotected intracerebral aneurysm and hematomyelia.117

Fluid and electrolyte management
Stroke patients should have a balanced fluid and electrolyte status to avoid plasma volume contraction, raised hematocrit and impairment of blood rheology (sludging). Uncontrolled volume replacement leads to pulmonary edema, cardiac failure and cerebral edema. In such instances a central venous catheter is mandatory. Serious electrolyte abnormalities are rare in stroke. Hyponatremia may occur due to SIADH (Syndrome of inappropriate secretion of anti diuretic harmone) or due to excess release of atrial natriuretic factor (ANF).120 Cerebral salt wasting (CSW) syndrome is due to centrally mediated renal sodium wasting.121,122 Existence of CSW syndrome remains controversial.123 The relation between hyponatremia, natriuresis and volume depletion is emphasized by many studies.121,124 SIADH is managed by fluid restriction or hypertonic saline, whereas normovolemia should be maintained along with oral salt supplementation if excess ANF is suspected.

Nosocomial infections
There are very few studies on the prevalence and incidence of nosocomial infections in neurointensive care units. The reported incidence varies.125 Review of the available literature from India shows an incidence of 18-39 %.126,127 Stroke patients are at high risk for silent aspiration, with pneumonia contributing to 34% of stroke deaths.128 Careful evaluation of cough and gag reflexes and a thorough swallowing is essential. Antibiotics are only recommended if the patient develops signs and symptoms of infection.129 Intubated patients have 7- 21 fold higher rate of pneumonia.130,131 The common organisms are staphylococcus, pseudomonas, enterobacter and klebsiella. Initial antibiotics recommended are a combination of third generation cephalosporins and aminoglycoside. Urinary tract infections are the commonest nosocomial infections with a reported incidence of 30-40%.132 Indwelling catheter increases the risk by 4-7 times.133 Commonest organisms are gram-negative aerobic bacilli and they are usually polymicrobial, followed by the fungi. Blood stream infections are also common in ICU set up. They are often due to coagulase negative staphylococcus followed by gramnegative organisms and candida. Nosocomial septicemia increases the risk of fatality by 25-50%.134 Empirical treatment should include vancomycin plus third generation cephalosporins, pending the culture report.

Decubitus ulcers
Frequent turning of immobilized patients is useful for prevention of pressure sores. The skin of the incontinent patient must be kept dry. Air or fluid filled mattress system should be used. If the decubitus ulcers does not respond to conservative therapy antibiotic therapy may be given for several days preceding surgical debridement.

Pharmacotherapy of acute ischemic stroke

Platelet inhibitors : The results of two large randomized, non blinded intervention studies, namely International Stroke Trial (IST) and Chinese Acute Stroke Trial (CAST)135,136 indicate that aspirin given within 24-48 hours after stroke seems to significantly reduce mortality and rate of recurrent stroke. The positive effect of aspirin may be due to its effect on the infarct itself or due to prevention of recurrent infarction or because of anti inflammatory effect of aspirin. Use of heparin, low molecular heparin or heparinoids in treatment of acute stroke is not recommended, because several studies failed to show an overall benefit (IST, The TOAST publication Committee).135,137 Little benefit even if observed was counterbalanced by increased number of hemorrhagic complications. Treatment of stroke in progression depends on an understanding of the pathophysiology of the stroke and the mechanism of progression, whether due to progressive thrombosis or progressing edema. Anticoagulation is considered the standard therapy for stroke caused by basilar artery thrombosis or stenosis and arterial dissections, although there is little evidence to support its use in either situation.

Thrombolytic therapy : Thrombolytic therapy with rtPA (0.9 mg/kg body weight) given within 3 hours after stroke onset is the recommended treatment of acute ischemic stroke.46 Intra-arterial treatment of acute middle cerebral artery occlusion in a 6-hour window period using pro-urokinase has also been shown to result in significantly improved outcome.138


Most patients with acute stroke do not require ICU care. It is essential to identify those patients who need close hemodynamic and airway monitoring. Patients who are likely to deteriorate and those receiving thrombolytic therapy should be admitted in ICU. As the treatment and prognosis in stroke patients are codetermined by underlying and associated systemic diseases these problems should be treated with appropriate medical therapies. Complications, which arise in ICU, should be identified and treated accordingly, to ensure better outcome. Thrombolysis with intravenous rtPA within 3 hours is recommended for suitable patients of ischemic stroke. In nonthrombolysed patients, Aspirin administered within 24-48 hours of stroke onset is the recommended treatment.


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