Q J Med 2001; 94: 167-172
© 2001 Association of Physicians
Commentary |
Management of acute physiological parameters after stroke
From the Department of Public Health Sciences, Guy's, King's and St Thomas' School of Medicine, London 1 Department of Elderly Care, Guy's and St Thomas' Hospital, London, UK
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Summary |
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 Top Summary IntroductionOxygenationHydrationGlucose controlBody temperatureBlood pressure controlConclusionReferences |
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Considerable effort has been directed towards acute stroke research with numerous drug therapies being tried and tested. As yet there is still no routine treatment that is unequivocally effective in acute stroke. The development of stroke units has been a major breakthrough in reducing disability through co-ordinated rehabilitation, and new interest is being focussed towards limiting acute neurological deterioration through acute stroke units. Monitoring and attempting to stabilize acute physiological parameters within normal limits such as blood pressure, temperature, hydration status, glucose levels and oxygen saturations, has become standard practice for some acute stroke units. Strategies to correct hypertension, hypotension, dehydration, hyperglycaemia, pyrexia and hypoxia may potentially reduce neuronal damage in the acute phase of stroke and subsequently improve functional outcome and survival. Whether we require large prospective randomized controlled trials to test whether these specific interventions are to be used in mainstay practice is unclear.
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Introduction |
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There has been considerable interest in various strategies to reduce neuronal injury and subsequent disability after stroke, such as thrombolysis and neuroprotection. However, one of the major successful developments in stroke over the last decade has been the birth of dedicated stroke units.1 Randomized controlled trials comparing stroke units treating patients in the acute and rehabilitation phase versus conventional care found considerable reductions in early death in patients managed in stroke units.2,3 The reduction in early death is believed to be due to monitoring and control of abnormal physiological parameters such as hypotension, hyperglycaemia, hypoxia, pyrexia and hydration in the acute phase, which may have aggravated cerebral damage. Significant differences in the management of acute physiology during the first 2 weeks of admission included the use of intravenous saline in the first 24 h, antipyretic and antibiotic medications, oxygen therapy and insulin infusions.2,3
Monitoring of acute physiological parameters with treatments aimed at maintaining physiological homeostasis also reduced early neurological progression in a pilot study.4 There is now experimental evidence suggesting that control of these abnormal physiological parameters acts as a form of neuroprotection which may potentially improve the viability of ischaemic neuronal tissue.5 This policy is now recommended by a European review of critical care in stroke.6 This article explores the influence of physiological parameters on stroke, and their subsequent management, based on the evidence available.
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Oxygenation |
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Oxygen content of the brain is dependent upon two factors: cerebral blood flow and arterial oxygen content. Normal cerebral blood flow is 50 ml/100 g/min, but when cerebral blood flow drops to 25 ml/100 g/min, neurones become electrically silent but remain potentially viable for several hours—the region known as the ischaemic penumbra.7 If cerebral blood flow falls below a critical level of 10 ml/100 g/min, irreversible damage occurs, with its ensuing metabolic derangement, including lactic acid production, glutamate release, depletion of adenosine triphosphate and entry of sodium and calcium into cells, leading to cytotoxic oedema and mitochondrial failure, respectively.8 Hypoxia following stroke results in anaerobic metabolism and depletion of energy stores, thereby worsening brain injury. Stroke patients are at risk from hypoxia due to abnormalities in respiratory function such as hypoventilation, aspiration pneumonia, atelectasis, Cheyne-Stokes respiration and pulmonary embolism.9–11
Improving oxygen content may therefore prevent further neurological deterioration in stroke. Evidence shows that stroke patients have lower oxygen saturations compared to matched controls, and that positioning patients upright will improve oxygen saturations as well as reducing intracranial pressure.12 It has been suggested that supplemental oxygen should be administered if oxygen saturations are below 95%.13
The use of supplemental oxygen for non-hypoxic patients is however more controversial. In animal models, highly enriched oxygen atmospheres increase mortality.14,15 Mitochondrial respiration is impaired after ischaemia, and it has been suggested that high oxygen concentrations increase the formation of oxygen free radicals during reperfusion, which induces further neuronal damage by lipid peroxidation.15 Hyperoxia also induces cerebral vasoconstriction, which may cause a reduction in cerebral blood flow.16 A small study by Nighoghossian and colleagues demonstrated that hyperbaric oxygen worsened stroke outcome.17 A recent quasi-randomized controlled study by Ronning and colleagues showed that routine (100%) oxygen supplementation for 24 h after stroke onset had no benefit in survival.18 However, in a subgroup of minor to moderate stroke patients, this intervention worsened survival at 7 months. Explanations given to support these findings included that of free radical oxygen formation during reperfusion causing further tissue injury. Supplemental oxygen was less harmful to patients with severe stroke, probably because they were more likely to have impaired respiration and therefore to benefit from oxygen therapy, and also because they had insufficient reperfusion of the ischaemic areas to succumb to the potential harmful effects. The study concluded that supplemental oxygen should not be routinely given to non-hypoxic patients with minor or moderate strokes. Further research is still required to assess the effects of using supplemental oxygen routinely in patients with severe stroke who are not hypoxic.
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Hydration |
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The majority of strokes occur in the elderly, who are more prone to disturbances in water balance than their younger counterparts. Considerable variation in water homeostasis occurs in stroke, with some patients being over-hydrated and other under-hydrated.19 Initial dehydration is frequently hyperosmolar, caused by an inadequate intake of water due to drowsiness or dysphagia, a reduction in thirst, or the presence of infection. Dehydration, leading to a rise in haematocrit and a reduction in blood pressure, can worsen the ischaemic process during stroke.20 Dehydration is also an important predisposing factor in stroke recurrence.21 Stroke patients with high plasma osmolality levels on admission have worse survival at 3 months.22 O'Neill and colleagues also concluded that a standard regimen for fluid input in acute stroke was inappropriate, and that fluid management required a more systematic approach with regular assessment of clinical and biochemical markers of dehydration.19 Conventional wisdom previously was directed at keeping stroke patients under-filled in order to prevent cerebral oedema, but studies have shown that early intervention with intravenous saline may have contributed to improving functional ability in stroke patients managed in a multidisciplinary environment.3
It was hypothesized that routine use of saline infusions in the first 24 h may have improved cerebral blood flow by limiting dips in systemic arterial blood pressure and preventing dehydration. Haemodilution can also affect cerebral blood flow and cerebral haemodynamics by altering plasma viscosity,23 however trials of haemodilution have not shown any clear benefits as yet and require further investigation.24
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Glucose control |
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Some 20–50% of acute stroke patients are hyperglycaemic on presentation,25 and 8–20% of patients presenting with stroke are diabetic.26 Various mechanisms have been suggested to explain the worse prognosis in diabetic and hyperglycaemic patients. These patients have chronic impairment of cerebral blood flow and cerebral autoregulation, reduced leukocyte and erythrocyte deformability, increased thrombotic states and endothelial cell activation.27
Meyers and Yamaguchi have demonstrated that animals made hyperglycaemic prior to cerebral ischaemia have more severe neurological impairments and brain damage than their normoglycaemic counterparts.28 The mechanism by which hyperglycaemia influences damage is complex. Experimental evidence suggests that the build-up of lactic acid in the ischaemic penumbra is pivotal in this process.29 Ischaemia leads to a reduction in oxidative glucose metabolism, resulting in production of lactic acid locally, which induces damage to neurones, glial cells and endothelial cells. Lactic acidosis also leads to vasogenic oedema, which impairs collateral flow and microcirculation.30 Hyperglycaemia increases lactic acid production by increasing the available glucose for anaerobic glucose metabolism, and also by inhibiting mitochondrial respiration. Patients with hyperglycaemic cortical ischaemic strokes have higher admission serum neurone-specific enolase, an enzyme released from injured neurones, compared with normoglycaemic patients.31
It is well established that diabetic patients have worse survival and slower recovery after stroke compared with non-diabetic patients.32,33 Most studies agree that high glucose levels after stroke are associated with poor outcome in non-diabetic patients,34–37 and this generally holds true with diabetic patients.39 However one study by Toni and colleagues suggested that hyperglycaemia may be beneficial in a subgroup of stroke patients.38 This benefit may depend on the presence of a collateral blood supply to the ischaemic penumbra. If collateral blood flow is poor, then it appears that hyperglycaemia may increase brain damage. However if collateral blood flow is good, then additional glucose may be beneficial.27 Previously, a number of studies have suggested that the hyperglycaemic response after stroke in non-diabetics was a stress response relating to initial stroke severity, as demonstrated by the correlation of glucose levels with cortisol and catecholamines levels.40,41 Other studies have suggested that hyperglycaemia influences stroke outcome independently of stroke severity and diabetic status.25,42,43 Weir and colleagues demonstrated that plasma glucose >8 mmol/l after acute stroke predicted poorer chances of survival and independence.25
To unravel the cause and effect issue of hyperglycaemia and stroke outcome, a clinical trial of active control of plasma glucose may be required.44 Hyperglycaemia is seen as a reflection of relative insulin deficiency, and a randomized controlled trial of normalizing glucose levels in patients with myocardial infarction using insulin has shown benefit.45 At present it is unclear how intensively glucose levels should be lowered, and whether the risks of hypoglycaemia can be avoided. Certainly, intravenous solutions containing glucose should be avoided in the acute phase of stroke. A pilot study addressing the safety of insulin infusions in stroke patients with moderate hyperglycaemia has now been addressed.46 Determining the effect of controlling hyperglycaemia after stroke may require a large prospective trial, but some would argue that the existing data is sufficient to recommend the importance of maintaining normoglycaemia acutely after stroke.
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Body temperature |
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Numerous animal studies have suggested that hyperthermia post stroke is detrimental to stroke recovery.47–49 Human studies have reported similar findings.50–53 A meta-analysis by Hajat and colleagues suggested that a temperature >37.0 °C to
38.0 °C in the first week was significantly associated with an increase in mortality and morbidity.54 Mechanisms for hyperthermia-induced brain damage include neurotransmitter release, free radical formation and impaired recovery of brain metabolism.55,56 An acute-phase response, disturbance of central mechanisms of temperature control or the presence of infection may explain elevated temperature after stroke. Infection post stroke may be associated with a more severe deficit, and it has been suggested that approximately 20% of elevated temperatures are attributable to infection.51 Since small changes of elevated temperature may aggravate neurological deterioration, it may be important to maintain normothemia. Although there are no clinical data about the usefulness of normalizing temperature with antipyretics, recommendations have been made to maintain normothermia at 36.0–37.0 °C with antipyretics and antibiotics where appropriate.57
Encouraging results from a non-randomized controlled trial inducing hypothermia in head injury patients have demonstrated improved neurological outcomes at 3 and 6 months, compared to patients who underwent normothermic treatment.58 Whether these results can be reproduced in stroke patients remains to be seen.
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Blood pressure control |
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TopSummaryIntroductionOxygenationHydrationGlucose controlBody temperatureBlood pressure controlConclusionReferences |
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The management of hypertension in the acute phase of stroke remains controversial. Approximately 30% of patients have a history of hypertension prior to stroke and 80% have high blood pressure on presentation.59 Due to spontaneous falls in blood pressure over 4–10 days, approximately 60% are left normotensive.60 There are conflicting views on the prognostic significance of hypertension immediately following acute stroke.61–64 Robinson and colleagues demonstrated that an increase in systolic blood pressure by 10 mmHg after stroke significantly predicted poor outcome.65 Jorgensen and colleagues, however, demonstrated that the relative risk of stroke progression decreased by a factor of 0.66 for each 20 mmHg increase in systolic blood pressure.26
The mechanisms that contribute to raised blood pressure after stroke are multifactorial, including pre-existing hypertension, hospitalization stress, increased sympathetic nervous system activation, activation of the renin-angiotensin-aldosterone system and the Cushing's reflex.66 After acute stroke, cerebral autoregulation, which maintains cerebral blood flow with normal limits (55–60 ml/100 g/min) at systemic blood pressures between 60 and 125 mmHg, becomes impaired.67 Cerebral blood flow becomes dependent upon systemic blood pressure, such that reducing systemic blood pressure will reduce cerebral blood flow in the ischaemic penumbra. If cerebral blood flow is reduced below 12 ml/100 g/min, neuronal death is likely to occur. Patients with chronic hypertension also have impaired autoregulation, such that autoregulation occurs at higher systemic blood pressure limits between 120 and 160 mmHg.68 In these patients, if mean arterial blood pressure is reduced below 70 mmHg, brain hypoxia ensues. Therefore, initiating anti-hypertensive therapy may have a deleterious effect. This effect has been observed in clinical trials with calcium antagonists and angiotensin-converting-enzyme inhibitors.69,75 In contrast, severe hypertension may promote early brain oedema and increase the risk of haemorrhagic transformation.61
There is no agreed consensus on the treatment of hypertension following stroke, however there is evidence that hypertensive medication is still overused acutely, with approximately 50% of patients being treated acutely with anti-hypertensive therapy.70 There is a general agreement to withhold anti-hypertensive therapy acutely, although there are no defined levels at which emergency treatment is required.71 It has been suggested that if systolic blood pressure exceeds 220 mmHg, if mean arterial blood pressure exceeds 130 mmHg, or if the patients exhibits hypertensive encephalopathy, then short-acting agents that can be easily titrated, such as labetolol or enalapril, should be considered.6 At present, an acute reduction of blood pressure carries a risk of potentially worsening ischaemia in patients with cerebral infarction. An ongoing study studying the effects of glyceryl trinitrate patches versus placebo in ischaemic and haemorrhagic stroke patients is in progress.72 A randomized multi-centre controlled trail is also in progress to determine whether patients with minor stroke and mild to moderate hypertension benefit from perindopril or a thiazide diuretic (PROGRESS: Perindopril protection against recurrent stroke study).73 Further questions that also need to be addressed include: how should anti-hypertensive therapy be administered if at all; for how long; and to which type/s of patients.76
Low blood pressure is uncommon after stroke, and may be related to volume loss.78 From studies of head trauma, a mean arterial blood pressure <80 mmHg is usually associated with loss of cerebral autoregulation and decline in cerebral perfusion pressure.77 Some researchers have hypothesized that blood pressure should be increased to improve cerebral perfusion.79 Limiting excessive drops in diastolic blood pressure by routinely giving patients intravenous saline on admission may be an important element in acute stroke care.3 Vasopressive drugs such as phenylephrine and haemodiluting agents have also been used with some success.80
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Conclusion |
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TopSummaryIntroductionOxygenationHydrationGlucose controlBody temperatureBlood pressure controlConclusionReferences |
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All stroke patients should be entitled to a high standard of acute care within a specialist environment such as a stroke unit. A major component of acute stroke care should focus upon strategies to limit neurological damage within the ischaemic penumbra by controlling abnormal physiology. Numerous animal and human studies have now demonstrated that hypotension, hyperglycaemia, pyrexia, hypoxia and dehydration aggravate neuronal damage after stroke. The use of interventions to correct these parameters has been supported through stroke unit trials showing fewer rates of early death with early intensive monitoring and treatment. The rationale for specific interventions, however, lacks evidence from randomized controlled trials. This sometimes may be used as an excuse for non-intervention in the acute phase in stroke. Whether large randomized controlled trials are necessary or justifiable to ensure that these interventions become part of routine acute stroke care, is debatable.
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Notes |
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Address correspondence to Dr A. Bhalla, Department of Public Health Sciences, Guy's, King's and St Thomas' School of Medicine, 42 Weston Street, London SE1 3DQ. e-mail: bhalla{at}ajay1.freeserve.co.uk
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