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Management of medical complications of stroke
Management of Medical Complications of Stroke Jos6 Biller, MD, and James T. Patrick, MD, PhD Approximately 500,000 people suffer a new or recurrent stroke annually; of the 350,000 survivors, approximately 31% require assistance with care and 71% have impaired vocational capacity; thus, the mortality and morbidity from stroke are very great. Most strokes are ischemic in origin, caused by atherosclerosis or blood clots occluding large and small arteries supplying the brain. Assuming the patient survives the ictal event--ischemic or hemorrhagic stroke--then mortality derives from complications including herniation syndromes, pneumonia, or myocardial infarction; morbid complications include seizures and behavioral changes. Minimizing or preventing these medical complications will increase the opportunity for the patient to be restored to his or her former functional and environmental status. 1 The following discussion briefly addresses the treatment and prevention of medical complications attending acute stroke.
Respiratory Nasotracheal and Nasogastric Tubes A not infrequent complication of large-bore nasotracheal tubes and nasogastric tubes is sinusitis, which may lead to sepsis. Treatment consists of discontinuing the nasogastric and nasotracheal tubes, decongestants, antibiotics, and drainage if indicated/
Nasoenteric Tubes Cuffed endotracheal and tracheostomy tubes are not protective from nasoenteric tube misplacement. Complications of nasoenteric tubes include inadvertent tracheobronchial incubation and pneumothorax as a result of puncturing of the pleura. 3
Pneumonia Death of pneumonia occurs in 15% to 25% of acute stroke patients. It is the most common cause of nonneuroFrom the Department of Neurology, Indiana University School of Medicine, Indianapolis,IN; and Capital Neuroscience,Raleigh, NC. Address reprint requests to Jos6 Biller, MD, Department of Neurology, Indiana UniversitySchoolof Medicine, EmersonHall, Room 125, 545 Barnhill Dr, Indianapolis,IN 46202-5124. Copyright 9 1997by National StrokeAssociation 1052-3057/97/0604-001453.00/0
logical death, with a peak incidence at 2 to 4 weeks. 4 Many cases of pneumonia are caused by chronic aspiration of oropharyngeal contents. 5 Pending demonstration of intact oropharyngeal function, oral feedings are withheld. If dysfunction is present, then a temporary enteral feeding tube is placed. Once acute aspiration pneumonia is diagnosed, empiric treatment is initiated pending identification of the infectious agent. Multiple antibiotics may be required. The more common agents include Pseudomonas aeruginosa, Escherichia coil, Staphylococcus aureus, and Klebsiella pneumoniae; less common agents include species of Serratia, Proteus, and anaerobes.
Neurogenic Puhnonand Edema Neurogenic pulmonary edema is a form of noncardiogenic pulmonary edema that may follow head injury, status epilepticus, subarachnoid hemorrhage, ischemic stroke, or other conditions associated with increased intracranial pressure. Treatment includes optimization of hemodynamic and oxygenation status using positive end-expiratory pressure (PEEP) and alpha-adrenergic blockers. 6
Cardiac Cardiac dysfunction is frequently associated with stroke; it may be the cause of, coexistent with, or a consequence of stroke. Cardiac dysfunction can manifest as electrocardiogram (ECG) changes, arrhythmias, or myocardial ischemia. Cardiac dysfunction occurs with ischemic stroke, intraparenchymal hemorrhage, and subarachnoid hemorrhage. Because of the high frequency of stroke-associated cardiac dysfunction, cardiac monitoring for 24 to 48 hours after hospital admission is indicated. If ECG changes occur, then serial creatine kinase and lactate degrydrogenase isoenzymes are obtained. Ischemic cardiac changes are usually treated with troponin levels or nitrates and antithrombotics. 7
Vascular Blood Pressure The blood pressure should be measured frequently or continuously monitored in stroke patients during the first 48 to 72 hours. Arterial hypertension immediately after
Journal of Stroke and Cerebrovascular Diseases, Vol. 6, No. 4, 1997: pp 217-220
217
BILLER AND PATRICK
218 stroke is a common occurrence. Usually the blood pressure spontaneously returns to the prestroke level within a few days. Management of the usually transient hypertension is controversial. 8,9 The objective is to maintain adequate cerebral blood flow (CBF) in the presence of impaired autoregulation. Assuming that cerebrovascular resistance is minimal, then CBF is directly proportional to cerebral perfusion pressure (CPP), which is the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). Thus, in the stroke patient, decreasing the MAP can significantly reduce CBF. A CPP of at least 70 mmHg should be maintained. If urgent blood pressure reduction is indicated, all efforts must be taken to avoid compromising the function of vital organs. We generally favor the use of repetitive intravenous minibolus injections of labetalol, starting with 10 mg over I to 2 minutes; the dose may be repeated or doubled every 10 to 20 minutes until a satisfactory blood pressure reduction is achieved or until a cumulative dose of 300 mg has been administered. Labetalol is contraindicated in patients with asthma, congestive heart failure, and greater than first-degree heart block. Recent studies indicate that sodium nitroprusside causes cerebral vasodilation and may increase ICP.
Venous Thrombosis and Pulmonmad Embolism Lower-extremity venous thrombosis is a common occurrence in hemiplegic stroke patients. In the absence of prophylaxis, deep venous thrombosis (DVT) develops in 60% to 75% of these patients, and lethal pulmonary embolism (PE) occurs in 5% of them. Treatment of acute DVT or PE consists of intravenous heparin (activated partial thromboplastin time 1.5 to 2.5 times control) followed by oral warfarin, which is continued for approximately 6 months. Indications for inferior vena cava plication include a contraindication to anticoagulation or recurrent emboli despite adequate anticoagulation. DVT prophylaxis is with low-dose (10,000 to 15,000 units/day) subcutaneous heparin. If anticoagulant treatment is contraindicated, then intermittent pneumatic compression of the lower extremities is recommended. ~~
Central Nervous System Cerebral Edema Cerebral edema with attendant herniation is the leading cause of death within the first week after ischemic or hemorrhagic stroke. Silver et aP reported mortality based on the type and location of the stroke: ischemic supratentorial, 15%; and infratentorial, 10%; and hemorrhagic, supratentorial, 58%; and infratentorial, 31%. Traditional treatment of increased ICP associated with stroke is shown in Table 1. Mannitol decreases blood viscosity and reduces elevated ICP. The acute administration of manni-
tol elevates blood volume and plasma osmolality before diuresis is achieved and blood volume is reduced. 11,~2The concomitant administration of loop diuretics may enhance its beneficial effect in reducing increased ICP. Steroids have not proven useful and may increase morbidity.13 Barbiturates appear to be ineffective in achieving a favorable outcome in stroke patients with elevated intracranial pressure. For cerebellar strokes with edema and herniation, ventriculostomy or posterior fossa decompression may be life saving.
Seizures Poststroke seizures occur in 5% to 20% of patients. Monotherapy with conventional antiepileptic drugs is usually successful. 14Because of its effects on platelets, we avoid the use of divalproex sodium (Depakote; Abbott Laboratories, North Chicago, IL) in patients with hemorrhagic stroke.
Behavioral Changes Depression occurs in 26% to 60% of stroke patients. Depression is more frequent with frontal lobe strokes (left greater than right), and it is more severe whenever strokes
Table 1. Medical management guidelines of elevated ICP in patients with stroke Correction of factors exacerbating increased ICP Hypercarbia Hypoxia Hyperthermia Acidosis Hypotension Hypovolemia Positional Avoid head and neck positions compressing jugular veins Avoid flat supine position. Elevate head of bed 15-30 degrees Medical therapy Endotracheal intubation and mechanical ventilation, if GCS <8 Hyperventilate to a PaCo2 of 25-28 mmHg (if herniating); gradual withdrawal Hyperosmolar therapy with mannitol (20% solution), 1 g/kg over 30 minutes Maintenance dose 0.25-0.5 g/kg over 30-60 minutes every 4-6 hours, depending on clinical course, serum osmolality, volume status, and ICP measurements; g gradual withdrawal Fluid restriction Avoid glucose solutions. Use normal saline. Maintain euvolemia. Replace urinary losses with normal saline in patients receiving mannitol Abbreviations: GCS, Glasgow Coma Scale; PaCo2, arterial carbon dioxide pressure.
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MANAGEMENT OF MEDICAL COMPLICATIONS OF STROKE
are closer to the frontal pole. is In the absence of treatment, depression will persist for many months and impede rehabilitative efforts. Treatment includes a coordinated effort from the medical team and family support group. Choice of antidepressant drug is based on the side effect profile of the medication and the individual patient variables. Pharmacotherapy with a slow titration of nortriptyline or selective serotonin reuptake inhibitors is frequently useful. Poststroke aphasia and neglect may be improved by bromocriptine.
Peripheral Nervous System The peroneal nerve may be compressed against the head of the fibula, resulting in foot drop. Ulnar nerve compression at the elbow may occur, especially in wheelchair-bound patients. Traction brachial plexopathy may occur from a paretic subluxed shoulder.
Fluid, Electrolytes, and Glucose An intravenous line is used for the administration of fluids, in the form of normal saline, and for the administration of emergency drugs if needed. Hyponatremia can occur as a result of the syndrome of inappropriate antidiuretic hormone (SIADH) secretion or a central salt wasting syndrome. 16Symptoms of hyponatremia include lethargy, cramps, and seizures. Treatment of asymptomatic patients with SIADH includes fluid restriction; in symptomatic euvolemic patients with SIADH, isotonic or hypertonic saline is given with furosemide to increase the serum sodium level by no more than I m E q / L per hour to 120 or 125 mEq/L. Patients with central salt wasting have decreased blood volumes; infusions of isotonic saline, colloids, and packed red blood cells may be required to restore circulating blood volume and normalize serum sodium. Diabetes mellitus is one of the major risk factors for ischemic stroke, affecting at least 15 million Americans. Hyperglycemia may exacerbate ischemic stroke by increasing anaerobic metabolism, with attendant lactic acid production, and altering phosphorus metabolism. 17 The presence of hyperglycemia affects the severity of acute ischemic stroke, the degree of recovery, and the risk of early stroke recurrence. In addition, high serum glucose levels intensify the risk of brain swelling and mortality after stroke. It is recommended that glycemia be maintained at or below 125 to 150 mg/dL.
Gastrointestinal Oropharyngeal dysphagia increases the risk of aspiration and occurs in approximately 30% of patients with stroke, s Standardized evaluation by a trained specialist should be performed. Therapy should address head
position, selection of foods, and avoidance of aspiration. Tube feedings may be needed in some patients. Bowel incontinence may occur because of loss of sensation and sphincter control. Increasing fiber in the diet and the use of diapers to minimize skin maceration is recommended. Constipation may initially occur because of adynamic ileus. A bowel regimen, including stool softeners, laxatives, suppositories, and enemas, is recommended to avoid impaction. Stress ulcers occur in stroke patients; if no prophylactic treatment is given, hemorrhages occur within 7 days after the precipitating event. Prophylaxis with H2 receptor antagonists, antacids, or sucralfate is recommended. Sucralfate also may decrease nosocomial pneumonia in ventilator-dependent patients. TM
Urinary Urinary retention and incontinence occur in stroke patients because of loss of volitional control or sphincter dyssynergy. Incontinence may lead to urinary tract infection. Indwelling catheters should be avoided if possible; eventually they cause significant bacteriuria. In the presence of an indwelling catheter, treatment of asymptomatic bacteriuria is usually not indicated. However, for significant clInical infection with pyuria and fever, treatment is recommended. 19
Dermatologic Stroke patients often develop pressure sores. Pressure sores, caused by compressive ischemia of the skin and subcutaneous tissues, are avoided by frequent (every 2 hours or more) repositioning of the head, trunk, and extremities. 20
Contrast Media Reactions Stroke patients with a history of reactions to contrast media requiring angiographic procedures should be pretreated with oral prednisone, diphenhydramine, and ephedrine, and should be evaluated with nonionic contrast agents.
References 1. Silver FL, Norris JW, Lewis AJ, Hachinski VC. Early mortality following stroke: a prospective review. Stroke 1984;15:492-6. 2. Perlman D, Caplan ES. Nosocomial sinusitis: a new and complex threat. J Crit Ill 1987;2:19-25. 3. Carey T, Holcombe B. Endotracheal intubation as a risk factor for complications of nasoenteric tube insertion. Critical Care Med 1991;19:427-9. 4. Bounds JV, Wiebers DO, Whisnant JP, et al. Mechanisms and timing of deaths from cerebral infarction. Stroke 1981;12:474-7.
BILLER AND PATRICK
220
5. Homer F, Massey EW, Riski FE, et al. Aspiration following stroke: clinical correlates and outcome. Neurology 1988;38:1359-62. 6. Theodore J, Robin ED. Pathogenesis of neurogenic pulmonary edema. Lancet 1975;2:749-51. 7. Oppenheimmer SM, Hachinski VC. The cardiac consequences of stroke. Neurol Clin 1992;10:167-76. 8. Hayashi M, Kobayashi H, Kawano H, et al. Treatment of systemic hypertension and intracrardal hypertension in cases of brain hemorrhage. Stroke 1988;19:314-21. 9. Adams HP Jr, Brott TG, Crowell RM, et al. Guidelines for the management of patients with acute ischemic stroke. A Statement for Healthcare Professionals from a Special Writing Group of the Stroke Council, American Heart Association. Stroke 1994;90:1588-1601. 10. McCarthy ST, Turner JJ, Robertson D, et al. Low dose heparin as a prophylaxis against deep vein thrombosis after acute stroke. Lancet 1977;2:800-1. 11. Muizelaar JP, Wei EP, Kontos HA, et al. Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes. J Neurosurg 1983;59:822-8. 12. Muizelaar JP, Lutz HA III, Becker DP. Effect of mannitol on ICP and CBF and correlation with pressure autoregu-
13. 14. 15. 16. 17.
18.
19. 20.
lation in severely head-injured patients. J Neurosurg 1984;61:700-6. Norris JW: Steroid therapy in acute cerebral infarction. Arch Neurol 1976;33:69-71. Olsen TS, Hogenhaven H, Thage O. Epilepsy after stroke. Neurology 1987;37:1209-11. Robinson RG, Starr LB, Kubos KL, et al. A two-year longitudinal study of post-stroke mood disorders: Findings during the initial evaluation. Stroke 1983;14:736-41. Bartter FC, Schwartz WB: The syndrome of inappropriate secretion of antidiuretic hormone. Am J Med 1967;42:790806. Pulsinelli W, Levy DE, Sigsbee B, et al. Increased damage after ischemic stroke in patients with hyperglycemia with or without established diabetes mellitus. Am J Med 1983;74:540-3. Driks MR, Craven DE, Celli BR, et al. Nosocomial pneumonia in intubated patients given sucralfate as compared with antacids or histamine type 2 blockers. N Engl J Med 1987;317:1376-82. Warren JW, Platt R, Thomas RJ, et al. Antibiotic irrigation and catheter-associated urinary tract infections. N Engl J Med 1978;299:570-3. Reuler J, Cooney T. The pressure sore: pathophysiology and principles of management. Ann Inern Med 1981;94: 661-6.
Respiratory Nasotracheal and Nasogastric Tubes A not infrequent complication of large-bore nasotracheal tubes and nasogastric tubes is sinusitis, which may lead to sepsis. Treatment consists of discontinuing the nasogastric and nasotracheal tubes, decongestants, antibiotics, and drainage if indicated/
Nasoenteric Tubes Cuffed endotracheal and tracheostomy tubes are not protective from nasoenteric tube misplacement. Complications of nasoenteric tubes include inadvertent tracheobronchial incubation and pneumothorax as a result of puncturing of the pleura. 3
Pneumonia Death of pneumonia occurs in 15% to 25% of acute stroke patients. It is the most common cause of nonneuroFrom the Department of Neurology, Indiana University School of Medicine, Indianapolis,IN; and Capital Neuroscience,Raleigh, NC. Address reprint requests to Jos6 Biller, MD, Department of Neurology, Indiana UniversitySchoolof Medicine, EmersonHall, Room 125, 545 Barnhill Dr, Indianapolis,IN 46202-5124. Copyright 9 1997by National StrokeAssociation 1052-3057/97/0604-001453.00/0
logical death, with a peak incidence at 2 to 4 weeks. 4 Many cases of pneumonia are caused by chronic aspiration of oropharyngeal contents. 5 Pending demonstration of intact oropharyngeal function, oral feedings are withheld. If dysfunction is present, then a temporary enteral feeding tube is placed. Once acute aspiration pneumonia is diagnosed, empiric treatment is initiated pending identification of the infectious agent. Multiple antibiotics may be required. The more common agents include Pseudomonas aeruginosa, Escherichia coil, Staphylococcus aureus, and Klebsiella pneumoniae; less common agents include species of Serratia, Proteus, and anaerobes.
Neurogenic Puhnonand Edema Neurogenic pulmonary edema is a form of noncardiogenic pulmonary edema that may follow head injury, status epilepticus, subarachnoid hemorrhage, ischemic stroke, or other conditions associated with increased intracranial pressure. Treatment includes optimization of hemodynamic and oxygenation status using positive end-expiratory pressure (PEEP) and alpha-adrenergic blockers. 6
Cardiac Cardiac dysfunction is frequently associated with stroke; it may be the cause of, coexistent with, or a consequence of stroke. Cardiac dysfunction can manifest as electrocardiogram (ECG) changes, arrhythmias, or myocardial ischemia. Cardiac dysfunction occurs with ischemic stroke, intraparenchymal hemorrhage, and subarachnoid hemorrhage. Because of the high frequency of stroke-associated cardiac dysfunction, cardiac monitoring for 24 to 48 hours after hospital admission is indicated. If ECG changes occur, then serial creatine kinase and lactate degrydrogenase isoenzymes are obtained. Ischemic cardiac changes are usually treated with troponin levels or nitrates and antithrombotics. 7
Vascular Blood Pressure The blood pressure should be measured frequently or continuously monitored in stroke patients during the first 48 to 72 hours. Arterial hypertension immediately after
Journal of Stroke and Cerebrovascular Diseases, Vol. 6, No. 4, 1997: pp 217-220
217
BILLER AND PATRICK
218 stroke is a common occurrence. Usually the blood pressure spontaneously returns to the prestroke level within a few days. Management of the usually transient hypertension is controversial. 8,9 The objective is to maintain adequate cerebral blood flow (CBF) in the presence of impaired autoregulation. Assuming that cerebrovascular resistance is minimal, then CBF is directly proportional to cerebral perfusion pressure (CPP), which is the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). Thus, in the stroke patient, decreasing the MAP can significantly reduce CBF. A CPP of at least 70 mmHg should be maintained. If urgent blood pressure reduction is indicated, all efforts must be taken to avoid compromising the function of vital organs. We generally favor the use of repetitive intravenous minibolus injections of labetalol, starting with 10 mg over I to 2 minutes; the dose may be repeated or doubled every 10 to 20 minutes until a satisfactory blood pressure reduction is achieved or until a cumulative dose of 300 mg has been administered. Labetalol is contraindicated in patients with asthma, congestive heart failure, and greater than first-degree heart block. Recent studies indicate that sodium nitroprusside causes cerebral vasodilation and may increase ICP.
Venous Thrombosis and Pulmonmad Embolism Lower-extremity venous thrombosis is a common occurrence in hemiplegic stroke patients. In the absence of prophylaxis, deep venous thrombosis (DVT) develops in 60% to 75% of these patients, and lethal pulmonary embolism (PE) occurs in 5% of them. Treatment of acute DVT or PE consists of intravenous heparin (activated partial thromboplastin time 1.5 to 2.5 times control) followed by oral warfarin, which is continued for approximately 6 months. Indications for inferior vena cava plication include a contraindication to anticoagulation or recurrent emboli despite adequate anticoagulation. DVT prophylaxis is with low-dose (10,000 to 15,000 units/day) subcutaneous heparin. If anticoagulant treatment is contraindicated, then intermittent pneumatic compression of the lower extremities is recommended. ~~
Central Nervous System Cerebral Edema Cerebral edema with attendant herniation is the leading cause of death within the first week after ischemic or hemorrhagic stroke. Silver et aP reported mortality based on the type and location of the stroke: ischemic supratentorial, 15%; and infratentorial, 10%; and hemorrhagic, supratentorial, 58%; and infratentorial, 31%. Traditional treatment of increased ICP associated with stroke is shown in Table 1. Mannitol decreases blood viscosity and reduces elevated ICP. The acute administration of manni-
tol elevates blood volume and plasma osmolality before diuresis is achieved and blood volume is reduced. 11,~2The concomitant administration of loop diuretics may enhance its beneficial effect in reducing increased ICP. Steroids have not proven useful and may increase morbidity.13 Barbiturates appear to be ineffective in achieving a favorable outcome in stroke patients with elevated intracranial pressure. For cerebellar strokes with edema and herniation, ventriculostomy or posterior fossa decompression may be life saving.
Seizures Poststroke seizures occur in 5% to 20% of patients. Monotherapy with conventional antiepileptic drugs is usually successful. 14Because of its effects on platelets, we avoid the use of divalproex sodium (Depakote; Abbott Laboratories, North Chicago, IL) in patients with hemorrhagic stroke.
Behavioral Changes Depression occurs in 26% to 60% of stroke patients. Depression is more frequent with frontal lobe strokes (left greater than right), and it is more severe whenever strokes
Table 1. Medical management guidelines of elevated ICP in patients with stroke Correction of factors exacerbating increased ICP Hypercarbia Hypoxia Hyperthermia Acidosis Hypotension Hypovolemia Positional Avoid head and neck positions compressing jugular veins Avoid flat supine position. Elevate head of bed 15-30 degrees Medical therapy Endotracheal intubation and mechanical ventilation, if GCS <8 Hyperventilate to a PaCo2 of 25-28 mmHg (if herniating); gradual withdrawal Hyperosmolar therapy with mannitol (20% solution), 1 g/kg over 30 minutes Maintenance dose 0.25-0.5 g/kg over 30-60 minutes every 4-6 hours, depending on clinical course, serum osmolality, volume status, and ICP measurements; g gradual withdrawal Fluid restriction Avoid glucose solutions. Use normal saline. Maintain euvolemia. Replace urinary losses with normal saline in patients receiving mannitol Abbreviations: GCS, Glasgow Coma Scale; PaCo2, arterial carbon dioxide pressure.
219
MANAGEMENT OF MEDICAL COMPLICATIONS OF STROKE
are closer to the frontal pole. is In the absence of treatment, depression will persist for many months and impede rehabilitative efforts. Treatment includes a coordinated effort from the medical team and family support group. Choice of antidepressant drug is based on the side effect profile of the medication and the individual patient variables. Pharmacotherapy with a slow titration of nortriptyline or selective serotonin reuptake inhibitors is frequently useful. Poststroke aphasia and neglect may be improved by bromocriptine.
Peripheral Nervous System The peroneal nerve may be compressed against the head of the fibula, resulting in foot drop. Ulnar nerve compression at the elbow may occur, especially in wheelchair-bound patients. Traction brachial plexopathy may occur from a paretic subluxed shoulder.
Fluid, Electrolytes, and Glucose An intravenous line is used for the administration of fluids, in the form of normal saline, and for the administration of emergency drugs if needed. Hyponatremia can occur as a result of the syndrome of inappropriate antidiuretic hormone (SIADH) secretion or a central salt wasting syndrome. 16Symptoms of hyponatremia include lethargy, cramps, and seizures. Treatment of asymptomatic patients with SIADH includes fluid restriction; in symptomatic euvolemic patients with SIADH, isotonic or hypertonic saline is given with furosemide to increase the serum sodium level by no more than I m E q / L per hour to 120 or 125 mEq/L. Patients with central salt wasting have decreased blood volumes; infusions of isotonic saline, colloids, and packed red blood cells may be required to restore circulating blood volume and normalize serum sodium. Diabetes mellitus is one of the major risk factors for ischemic stroke, affecting at least 15 million Americans. Hyperglycemia may exacerbate ischemic stroke by increasing anaerobic metabolism, with attendant lactic acid production, and altering phosphorus metabolism. 17 The presence of hyperglycemia affects the severity of acute ischemic stroke, the degree of recovery, and the risk of early stroke recurrence. In addition, high serum glucose levels intensify the risk of brain swelling and mortality after stroke. It is recommended that glycemia be maintained at or below 125 to 150 mg/dL.
Gastrointestinal Oropharyngeal dysphagia increases the risk of aspiration and occurs in approximately 30% of patients with stroke, s Standardized evaluation by a trained specialist should be performed. Therapy should address head
position, selection of foods, and avoidance of aspiration. Tube feedings may be needed in some patients. Bowel incontinence may occur because of loss of sensation and sphincter control. Increasing fiber in the diet and the use of diapers to minimize skin maceration is recommended. Constipation may initially occur because of adynamic ileus. A bowel regimen, including stool softeners, laxatives, suppositories, and enemas, is recommended to avoid impaction. Stress ulcers occur in stroke patients; if no prophylactic treatment is given, hemorrhages occur within 7 days after the precipitating event. Prophylaxis with H2 receptor antagonists, antacids, or sucralfate is recommended. Sucralfate also may decrease nosocomial pneumonia in ventilator-dependent patients. TM
Urinary Urinary retention and incontinence occur in stroke patients because of loss of volitional control or sphincter dyssynergy. Incontinence may lead to urinary tract infection. Indwelling catheters should be avoided if possible; eventually they cause significant bacteriuria. In the presence of an indwelling catheter, treatment of asymptomatic bacteriuria is usually not indicated. However, for significant clInical infection with pyuria and fever, treatment is recommended. 19
Dermatologic Stroke patients often develop pressure sores. Pressure sores, caused by compressive ischemia of the skin and subcutaneous tissues, are avoided by frequent (every 2 hours or more) repositioning of the head, trunk, and extremities. 20
Contrast Media Reactions Stroke patients with a history of reactions to contrast media requiring angiographic procedures should be pretreated with oral prednisone, diphenhydramine, and ephedrine, and should be evaluated with nonionic contrast agents.
References 1. Silver FL, Norris JW, Lewis AJ, Hachinski VC. Early mortality following stroke: a prospective review. Stroke 1984;15:492-6. 2. Perlman D, Caplan ES. Nosocomial sinusitis: a new and complex threat. J Crit Ill 1987;2:19-25. 3. Carey T, Holcombe B. Endotracheal intubation as a risk factor for complications of nasoenteric tube insertion. Critical Care Med 1991;19:427-9. 4. Bounds JV, Wiebers DO, Whisnant JP, et al. Mechanisms and timing of deaths from cerebral infarction. Stroke 1981;12:474-7.
BILLER AND PATRICK
220
5. Homer F, Massey EW, Riski FE, et al. Aspiration following stroke: clinical correlates and outcome. Neurology 1988;38:1359-62. 6. Theodore J, Robin ED. Pathogenesis of neurogenic pulmonary edema. Lancet 1975;2:749-51. 7. Oppenheimmer SM, Hachinski VC. The cardiac consequences of stroke. Neurol Clin 1992;10:167-76. 8. Hayashi M, Kobayashi H, Kawano H, et al. Treatment of systemic hypertension and intracrardal hypertension in cases of brain hemorrhage. Stroke 1988;19:314-21. 9. Adams HP Jr, Brott TG, Crowell RM, et al. Guidelines for the management of patients with acute ischemic stroke. A Statement for Healthcare Professionals from a Special Writing Group of the Stroke Council, American Heart Association. Stroke 1994;90:1588-1601. 10. McCarthy ST, Turner JJ, Robertson D, et al. Low dose heparin as a prophylaxis against deep vein thrombosis after acute stroke. Lancet 1977;2:800-1. 11. Muizelaar JP, Wei EP, Kontos HA, et al. Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes. J Neurosurg 1983;59:822-8. 12. Muizelaar JP, Lutz HA III, Becker DP. Effect of mannitol on ICP and CBF and correlation with pressure autoregu-
13. 14. 15. 16. 17.
18.
19. 20.
lation in severely head-injured patients. J Neurosurg 1984;61:700-6. Norris JW: Steroid therapy in acute cerebral infarction. Arch Neurol 1976;33:69-71. Olsen TS, Hogenhaven H, Thage O. Epilepsy after stroke. Neurology 1987;37:1209-11. Robinson RG, Starr LB, Kubos KL, et al. A two-year longitudinal study of post-stroke mood disorders: Findings during the initial evaluation. Stroke 1983;14:736-41. Bartter FC, Schwartz WB: The syndrome of inappropriate secretion of antidiuretic hormone. Am J Med 1967;42:790806. Pulsinelli W, Levy DE, Sigsbee B, et al. Increased damage after ischemic stroke in patients with hyperglycemia with or without established diabetes mellitus. Am J Med 1983;74:540-3. Driks MR, Craven DE, Celli BR, et al. Nosocomial pneumonia in intubated patients given sucralfate as compared with antacids or histamine type 2 blockers. N Engl J Med 1987;317:1376-82. Warren JW, Platt R, Thomas RJ, et al. Antibiotic irrigation and catheter-associated urinary tract infections. N Engl J Med 1978;299:570-3. Reuler J, Cooney T. The pressure sore: pathophysiology and principles of management. Ann Inern Med 1981;94: 661-6.