Perioperative care of a patient with stroke
© Veenith et al. 2010
Received: 16 June 2010
Accepted: 20 November 2010
Published: 20 November 2010
Strokes and TIAs, with their high cumulative mortality and morbidity rates, are occurring with increasing frequency in western population [1, 4]. As such, it is vital for clinicians to provide optimal medical management in the perioperative period for those patients with this common neurological problem. This review aims to highlight the importance of the perioperative period and the stages of pre-optimization that can be taken by the multi-disciplinary team to aid this [17–19]. The evidence suggests that there are significant physiological advantages to early invasive monitoring and high dependency care in these complex patients. These cohort of patients are at increased risk of development of respiratory, gastrointestinal, nutritional and electrolyte disturbances so a constant vigil should be exercised in early recognition and treatment.
Peri- and post-operative care of the patient with neurologic illness poses a clinical and logistical challenge for the team participating in the care of the patient. The management of patients with cerebrovascular disease undergoing surgery requires an understanding of the pathophysiological mechanisms involved. This enables appropriate selection of patients who are suitable for surgery, with pre-optimization and vigilance to avoid predictable complications, as well as continued evaluation to detect any peri-operative deterioration.
A Transient Ischaemic Attack (TIA) occurs when there is a change to the blood supply of an area of the brain resulting in a change in neurologic function lasting for less than 24 hours. If the neurological dysfunction persists for up to 72 hours, but resolves, this is termed a Reversible Ischaemic Neurological Defect (RIND). When the neurological dysfunction persists for more than 72 hours, it is categorised as a stroke.
i) Ischaemic and haemorrhagic stroke (CVA)
When evaluating a patient preoperatively with ischaemic or haemorrhagic stroke the following should be considered -
Underlying mechanisms of haemorrhagic and ischaemic stroke 3
Thrombus - from a ulcerated plaque in the carotid artery
Hypertension is the commonest - causing weakness of the vessel wall
Cardioembolism from Atrial fibrillation (AF)
Large vessel atherosclerosis causing a stroke by occlusion
Use of sympathomimetic drugs such as cocaine causing transient hypertension
Small deep perforating vessel arthrosclerosis causing lacunar stroke
Congenital Arterio-venous malformations, aneurysms
A venous clot, causing paradoxical embolism through a patent foramen ovale (PFO)
Uncommon such as tumours, vasculitis, bleeding diathesis and use of anticoagulants
Vasospasm of structurally normal vessels (e.g. sympathomimetic drug use)
Hypercoagulable state, operating with any of these mechanisms or independently
Risk factors for the development of stroke 3578910
Common traditional factors
Hypertension, previous transient ischaemic attacks, Smoking, Diabetes Mellitus, AF, Cardiovascular diseases (MI, angina, Peripheral vascular diseases) and heart failure
Common traditional factors
Male sex, age, hypertension, diabetes mellitus and alcohol intake.
Haemostatic factors - factor VIIIc and von Willebrand factor
Haemostatic factors - Use of the anticoagulants and antiplatlet agents
Non traditional factors - Waist hip ratio, Left ventricular hypertrophy, Apolipoprotein(a) levels and White cell counts suggestive of inflammation
Non traditional factors - Previous TIA's
Predictors of death for the haemorrhagic (predicting death and disability at 30 days) and ischaemic strokes (death and disability at 100 days) 611
Size and location
The volume of ICH and location
Right and left arm paresis at admission, lenticulostriate infarction
Age, sex, prior stroke and Diabetes
Severity at presentation
The Glasgow Coma Scale (GCS) on admission
National institutes of health Stroke Scale at admission and Rankin Scale 48-72 hours later
Fever, neurological complications.
Favourable predictors of ischaemic and haemorrhagic stroke 4
Location and good function at presentation
Mild neurological dysfunction
Mild neurological dysfunction
Low fibrinogen levels
Absence of AF as this predicts more Cardiovascular deaths
Risk factors increasing mortality following TIA
Risk factors for development of death following a TIA
Stroke in heavy smokers - > 40 per day (level comes to normal after 5 years of stopping)
Atrial Fibrillation -increasing risk about 5-fold
Diabetes, hypertension, MI and high cholesterol
Race - African American race has higher incidence
Conjugate equine oestrogen increased risk of ischemic stroke and TIAs by 55%
ii) Stroke: Transient ischaemic attacks
Transient ischaemic attacks are much more common than strokes and occur in up to one in fifteen patients over 65 years . The 90 day risk for a stroke after a TIA is 3% to 17.3% and is at its highest within the first 30 days after a TIA. Approximately half of patients who experience a TIA fail to report it to their healthcare providers [14–16]. The risk of dying after TIA is highest in the first 12 months.
Prevention of ischaemic strokes and the transient ischaemic attacks
Reduction strategies for the prevention of TIA and ischaemic strokes
Risk factor management
Class I, Level of Evidence A, Benefit has been associated with an average reduction of &10/5 mm Hg (Normal defined by JNC 7 criteria as 120/80 mmHg). Drugs should be optimised to the target patient (consider the cardiac history, DM etc)
Class I, Level of Evidence A, Rigorous control of hypertension and intensive lipid lowering treatment, any drugs appropriate and most often > 1 drug needed.
Class I, Level of Evidence A, Lifestyle modification, dietary guidelines and statins
Class I, Level of Evidence C, Strongly advise every patient with stroke or TIA to quit
Class I, Level of Evidence A. Heavy drinkers should eliminate or reduce their consumption of alcohol.(it is actually a J-shaped association between alcohol and ischemic stroke, with a protective effect in light or moderate drinkers and an elevated stroke risk with heavy alcohol consumption)
Class IIb, Level of Evidence C. BMI of between 18.5 and 24.9 kg/m2 and a waist circumference of < 35 in for women and < 40 in for men
Class IIb, Level of Evidence C. At least 30 minutes of moderate-intensity physical exercise
Class I, Level of Evidence A. TIA or ischemic stroke within the last6 months and severe (70% to 99%) carotid artery stenosis, CEA by a surgeon with a peri-operative morbidity and mortality of < 6%. Consider CEA for certain high risk candidates with moderate stenosis (50-99%). If the TIA preferably within 2 weeks of after TIA.
Carotid angioplasty and stenting may be suitable for some patients with symptomatic high-grade stenosis and factors that make CEA unfavourable.
Extracranial Vertebrobasilar Disease/Intracranial Atherosclerosis
Class IIb, Level of Evidence C Endovascular treatment - when patients are having symptoms despite medical therapies
Cardiogenic Embolism and PAF
Class I, Level of Evidence A, paroxysmal (intermittent) AF, anticoagulation with adjusted-Dose Warfarin (target INR, 2.5; range, 2.0 to 3.0). Aspirin to be given in those patients with a clear contra-indication to Warfarin.
Cardiogenic Embolism - LV thrombus
Oral anticoagulation is reasonable, aiming for an INR of 2.0 to 3.0 for at least 3 months and up to 1 year (Class IIa, Level of Evidence B)
Noncardioembolic ischemic stroke or TIA
(Class IIa, Level of Evidence A) Aspirin (50 to 325 mg/d), the combination of aspirin and extended-release dipyridamole, and clopidogrel are all acceptable options for initial therapy. Aspirin to clopidogrel increases the risk of haemorrhage and is not routinely recommended for ischemic stroke or TIA patients (Class III, Level of Evidence A).
Patent Foramen Ovale
PFO closure may be considered for patients with recurrent cryptogenic stroke despite optimal medical therapy (Class IIb, Level of Evidence C)
Initial assessment and treatment of ischaemic strokes 
Patients who have an acute TIA or stroke with a good recovery should be commenced on appropriate antiplatlet therapy and risk factors such as hypertension should be dealt with promptly prior to referral to a specialist neurovascular clinic. If there is evidence of more than one TIA in 24 hours, ideally the patient should be admitted to hospital and investigated as an inpatient.
Initial neurological assessment should focus on the area of the brain affected and imaging of the brain (typically CT) should be arranged as soon as possible (< 24 hours). Imaging should be performed as an emergency if there are any suggestions of high risk features such as anticoagulant treatment, bleeding tendency and depressed level of consciousness including unexplained progressive or fluctuating symptoms. Other worrying features include papilloedema, neck stiffness or fever and severe headache at onset. Indications for thrombolysis or early anticoagulation, which is discussed below, must be considered. Furthermore, in addition to routine the observations, which should include conscious level, blood pressure, pulse, heart rhythm, temperature, oxygen saturation and hydration; the patients should be screened for evidence of aspiration/swallowing difficulties. Baseline investigations should include a full blood count, clotting screen, blood sugar, urea and electrolytes and an electrocardiogram.
Indications for thrombolysis
Thrombolysis (e.g. alteplase) should be performed after consultation with an experienced physician and within three hours of the onset of imaging confirmed ischaemic stroke (Class I, Level of Evidence); intra-arterial thrombolysis should be reserved for centres with interventional neuroradiology services.
Acute treatment of intracerebral bleeds
Surgical intervention should be considered in cases of supratentorial haemorrhage with mass effect or posterior fossa/cerebellar haematoma. Neurosurgical opinion should be sought for cases of secondary hydrocephalus following the intracerebral bleed.
Acute treatment of Subarachnoid Haemorrhage (SAH)
Whilst trauma remains the commonest cause of SAH, ruptured intracranial aneurysms account for 80% of non-traumatic cases. However, it remains standard, that regardless of cause, all cases should be referred for neurosurgical consideration unless the patient is for palliative treatment only. SAH is treated with either endovascular coiling or an open clipping (depending on the centre experience and availability of interventional neuroradiologists/neurosurgeons). Acute complications such as hydrocephalus may require an external ventricular drain to stabilise the patient and assess potential for neurological recovery. A detailed discussion is outside the scope of this review .
Perioperative implications for patients with a history of stroke 
Patients with a history of stroke frequently have coexisting vascular disease. Therefore, the overall management aim is protection against further strokes as well as prevention of further damage to other organs.
These patients mostly have multiple vessel involvement including the coronary arteries. They are also likely to suffer from other co morbidities such as hypertension and/or diabetes mellitus. Chronic hypertension shifts the cerebral autoregulation curve to the right, rendering the patients vulnerable to the haemodynamic compromise and the stress associated with the surgery . Relative hypotension may increase the risk of end organ ischaemia. To avoid these complications invasive monitoring may be necessary in the perioperative period with consideration for high dependency care postoperatively.
Complications following the illness
Care is required to reduce the incidence of complications potentiated by the presence of focal neurological deficits, as well as those related to coexisting illnesses.
Respiratory complications following a CVA 
Alterations of respiratory control, mechanics, and pattern are common following a CVA and lead to gas exchange abnormalities. Central or obstructive sleep apnoea may occur. Immobility can cause further complications such as hypostatic or aspiration pneumonia and venous thromboembolism. Many of these patients would need admission to a critical care areas following surgery for these reasons.
GI complications 
These patients may be at increased risk of aspiration due to impaired swallowing, ineffective cough and reduced gastric emptying.
Poor nutritional intake following the stroke may lead to malnutrition and may be associated with poor survival and functional outcomes after the surgery.
Strokes are notoriously associated with electrolytic disturbances for a variety of reasons. These include poor nutritional intake , dyselectrolemia directly related to the stroke  (acutely and associated cardiac arrhythmias) and diuretics  used for the treatment of hypertension.
Drug therapy and perioperative period
The team should be mindful of the hypercoagulable state created by the withdrawal of the drugs (such as statins and antithrombotic antiplatlet aggregation drugs) prior to surgery. This is often necessary to minimise surgical complications related to bleeding, but may also occur as a result of fasting. The risks/benefits of withdrawing such drugs need to be considered on a patient by patient basis.
Stroke is the third leading cause of death in Europe  and has a cumulative mortality at 5 years of 60.1 . A TIA carries a 3-17.3% risk of subsequent stroke within 90 days . As well as mortality strokes confer a significant morbidity.
A careful approach must be taken to the evaluation of a patient who has had a previous stroke in determining whether they are fit for an unrelated surgical procedure. A multidisciplinary approach is required to first ascertain whether surgery is the most appropriate treatment option. This must take into account the estimated morbidity and mortality, the post-operative facilities available for rehabilitation, and of course the patient's wishes.
Pre-optimization is desirable in patients undergoing elective procedures. Following a stroke or TIA all relevant secondary prevention strategies should be addressed as per the latest American Heart Association (AHA)/American Stroke Association (ASA) guidelines of October 2010 . This should include risk factor management, medical therapies, and surgical interventions as appropriate.
Patients with a history of stroke tend to have co-existing vascular disease and are more likely to suffer from co-morbidities like diabetes mellitus, hypertension, and ischaemic heart disease. The peri-operative team should aim to protect the patient from risk of further stroke, as well as to limit any further organ damage from hypoperfusion in these high-risk individuals. As such invasive monitoring is desirable, and consideration should be made to possible high-dependency care post-operatively.
Complications secondary to stroke must be appreciated and addressed in the post-operative period. These include the risk of venous thromboembolism related to decreased mobility associated with stroke, which will be potentiated by most surgical procedures. Stroke patients also have an increased risk of aspiration pneumonia [23, 24]. Poor nutritional intake following the stroke may lead to malnutrition and may be associated with poor survival and functional outcomes after the surgery. Electrolyte abnormalities are commonly associated with strokes and may lead to dysrhythmias both peri- and post-operatively [24, 25]. If anti-platelet drugs are withdrawn for surgical considerations the team should be aware of the increased risk of thrombosis.
The patient with a history of stroke undergoing surgery is high-risk, and requires careful pre-operative evaluation, pre-optimaztion, and close monitoring for predictable post-operative complications.
- European Registers of Stroke Investigators: Incidence of stroke in europe at the beginning of the 21st century. Stroke 2009, 40:1557–63.View ArticleGoogle Scholar
- Wolf PA, Clagett GP, Easton JD, et al.: Preventing ischemic stroke in patients with prior stroke and transient ischemic attack: a statement for healthcare professionals from the Stroke Council of the American Heart Association. Stroke 1999, 30:1991–94.PubMedGoogle Scholar
- Cucchiara BL: Evaluation and management of stroke. Hematology Am Soc Hematol Educ Program 2009, 293–301.Google Scholar
- Hankey GJ, Jamrozik K, Broadhurst RJ, et al.: Five-year survival after first-ever stroke and related prognostic factors in the Perth Community Stroke Study. Stroke 2000, 31:2080–86.PubMedGoogle Scholar
- Ariesen MJ, Claus SP, Rinkel GJE, Algra A: Risk factors for intracerebral hemorrhage in the general population: a systematic review. Stroke 2003, 34:2060–65.View ArticlePubMedGoogle Scholar
- Broderick J, Connolly S, Feldmann E, et al.: Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Circulation 2007, 116:e391–413.View ArticlePubMedGoogle Scholar
- Ariesen MJ, Algra A, Warlow CP, Rothwell PM, Cerebrovascular Cohort Studies Collaboration (CCSC): Predictors of risk of intracerebral haemorrhage in patients with a history of TIA or minor ischaemic stroke. J Neurol Neurosurg Psychiatry 2006, 77:92–94.View ArticlePubMedGoogle Scholar
- Ohira T, Shahar E, Chambless LE, Rosamond WD, Mosley TH, Folsom AR: Risk factors for ischemic stroke subtypes: the Atherosclerosis Risk in Communities study. Stroke 2006, 37:2493–98.View ArticlePubMedGoogle Scholar
- Rodgers H, Greenaway J, Davies T, Wood R, Steen N, Thomson R: Risk factors for first-ever stroke in older people in the north East of England: a population-based study. Stroke 2004, 35:7–11.View ArticlePubMedGoogle Scholar
- Zodpey SP, Tiwari RR, Kulkarni HR: Risk factors for haemorrhagic stroke: a case-control study. Public Health 2000, 114:177–82.View ArticlePubMedGoogle Scholar
- Weimar C, Ziegler A, König IR, Diener HC: Predicting functional outcome and survival after acute ischemic stroke. J Neurol 2002, 249:888–95.View ArticlePubMedGoogle Scholar
- Matta BF, Menon DK, Turner JM (Eds): Cerebral Physiology for textbook of neuroanaesthesia and neurocritical care Textbook of neuroanaesthesia and critical care.: Cambridge; 2000:448.
- Johnston SC, Gress DR, Browner WS, Sidney S: Short-term prognosis after emergency department diagnosis of TIA. JAMA 2000, 284:2901–06.View ArticlePubMedGoogle Scholar
- Rosamond W, Flegal K, Friday G, et al.: Heart disease and stroke statistics--2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2007, 115:e69–171.View ArticlePubMedGoogle Scholar
- Rosamond W, Flegal K, Furie K, et al.: Heart disease and stroke statistics--2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008, 117:e25–146.View ArticlePubMedGoogle Scholar
- Thom T, Haase N, Rosamond W, et al.: Heart disease and stroke statistics--2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2006, 113:e85–151.View ArticlePubMedGoogle Scholar
- Sacco RL, Adams R, Albers G, et al.: Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of this guideline. Circulation 2006, 113:e409–49.PubMedGoogle Scholar
- Stroke - National clinical guideline for diagnosis and initial management of acute stroke and transient ischaemic attack (TIA) Royal College of Physicians 2008.
- Furie KL, Kasner SE, Adams RJ, et al.: Guidelines for the Prevention of Stroke in Patients With Stroke or Transient Ischemic Attack. A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2010.Google Scholar
- Birenbaum D: Emergency neurological care of strokes and bleeds. Journal of emergencies, trauma and shock 2010, 3:52–61.View ArticlePubMedGoogle Scholar
- Frost EA: Anaesthetic management of cerebrovascular disease. Br J Anaesth 1981, 53:745–56.View ArticlePubMedGoogle Scholar
- Rochester CL, Mohsenin V: Respiratory complications of stroke. Semin Respir Crit Care Med 2002, 23:248–60.View ArticlePubMedGoogle Scholar
- Schaller BJ, Graf R, Jacobs AH: Pathophysiological changes of the gastrointestinal tract in ischemic stroke. Am J Gastroenterol 2006, 101:1655–65.View ArticlePubMedGoogle Scholar
- Dennis M: Nutrition after stroke. Br Med Bull 2000, 56:466–75.View ArticlePubMedGoogle Scholar
- Fukui S, Katoh H, Tsuzuki N, et al.: Multivariate analysis of risk factors for QT prolongation following subarachnoid hemorrhage. Crit Care 2003, 7:R7–12.View ArticlePubMedGoogle Scholar
- Clayton JA, Rodgers S, Blakey J, Avery A, Hall IP: Thiazide diuretic prescription and electrolyte abnormalities in primary care. Br J Clin Pharmacol 2006, 61:87–95.View ArticlePubMedGoogle Scholar
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