Preventing complications_stroke_Jan090

ALBERTA PROVINCIAL STROKE STRATEGY (APSS) Preventing Complications of Stroke 01/09:01/10

TABLE OF CONTENTS PageINTRODUCTION ......................................................................................................................... 3LEARNING OBJECTIVES............................................................................................................ 41.0 HEMORRHAGIC TRANSFORMATION……….. .......................................................... ……52.0 CEREBRAL EDEMA ……….. ...................................................................................... ……63.0 DYSPHAGIA……...................................................................................................…….……74.0 ASPIRATION PNEUMONIA ........................................................................................……115.0 POST STROKE DEPRESSION………………..................................................................…126.0 SEIZURES……………….……….. .............................................................................. ……147.0 VISUAL NEGLECT……………….……….. ................................................................. ……158.0 URINARY INCONTINENCE….……………………….................................................... ……169.0 URINARY TRACT INFECTIONS….…………………………............................................ ……1710.0 DEEP VEIN THROMBOSIS.…………………………....................................................……1811.0 SHOULDER COMPLICATION……….……….. ...............................................................…1911.1 Shoulder Subluxation………….……….. ..............................................................……2011.2 Hemiparetic Shoulder Pain………….………............................................……2012.0 SPASTICITY……………..….. ........................................................................... ……2013.0 CARDIAC COMPLICATIONS…….………………………................................................. ……2113.1 Repolarization and ECG Abnormalities…………….….………………….......................... ……2313.2 Dysrhythmias…………….………..................................................................................... ……2413.3 Elevated Cardiac Enzymes……………….……………………............................................ ……2413.4 Myocardial Infarction……………….………………………................................................ ……2413.5 Neurogenic Cardiac Damage……………….………………………...................................... ……25QUICK REFERENCE TABLE……………….……….................................................. ……28REFERENCES……………….……….. ...................................................................... ……32STUDY QUESTIONS……………….……….. ............................................................ ……37ANSWER KEY……………….………......................................................................... ……42Information was produced and/or compiled by the Alberta Provincial Stroke Strategy and written permission is required prior to reprinting any of the material located within this document. 2

PREVENTING COMPLICATIONS OF STROKEINTRODUCTION Stroke is the number one cause of acquired long-term disability in the adult population and is the fourth leading cause of death in Canada. It is the most common neurological disease requiring admission to hospital (Alberta Provincial Stroke Strategy Blueprint, 2006). The cost of stroke in Alberta is approximately $200-$300 million annually. In Alberta, there are approximately 5500 new stroke cases each year and at present, 25,000 stroke survivors. The incidence of stroke will continue to rise as the population ages (Alberta Provincial Stroke Strategy Blueprint, 2006). Despite advances in stroke management, post-stroke complications continue to occur and impede the stroke survivor’s ability to recover. The frequency and type of post-stroke complications vary with the severity of neurological and functional deficits. One study revealed at least one medical complication in 95% of patients and at least one serious medical complication (immediately life threatening or resulting in hospitalization or death) occurring in 24% (Johnston et al, 1998). Approximately 50% of deaths after stroke are attributed to medical complications (Silver, 1984). As an example, from 1994 to 2002, 591 patients (5.1% of patients) in the Calgary Health Region with a primary discharge diagnosis of stroke developed in-hospital complications from pneumonia, pulmonary embolism or deep vein thrombosis (Field et al, 2004). The presence of post-stroke complications has a direct relation to length of hospital stay, poor outcomes, and increasing health care expenditures. 3

PREVENTING COMPLICATIONS OF STROKELEARNING OBJECTIVES Upon completion of this learning module, the participant will be able to: Describe the etiology, signs, symptoms, and management of the following post- stroke complications: • Hemorrhagic transformation • Cerebral edema • Dysphagia • Aspiration pneumonia • Post-stroke depression • Seizure • Visual Neglect • Urinary Incontinence • Urinary tract infections • Venous thromboembolism • Shoulder complications • Spasticity • Cardiac complications Concluding this learning module is a table that summarizes the foregoing. This learning module is developed for self-study. There are questions at the end of the module along with an answer key. 4

1. HEMORRHAGIC TRANSFORMATION Hemorrhagic transformation (or conversion) is a serious complication which may occur 1 – 2 days after an ischemic stroke. Hemorrhagic transformation results when bleeding takes place into the brain tissue already damaged by the ischemic stroke. It occurs in the following stages: 1. obstruction of a blood vessel by an embolism produces ischemic brain tissue and damages blood vessels 2. affected blood vessels are injured, edematous, and become “leaky” 3. when blood flow is restored to the injured blood vessels, a hemorrhage can occur in the area of these friable blood vessels. It is estimated that hemorrhagic transformation will occur in approximately 5% of patients with ischemic stroke. The likelihood of developing hemorrhagic transformation is influenced by the following: • the size and location of the infarct • the degree of collateral circulation • the use of anticoagulants and interventional therapy with thrombolytic agents – this is associated with a higher incidence of hemorrhagic transformation (AHA/ASA Guidelines for the Management of Adults with Ischemic Stroke, 2007) (Courtesy of the Internet Stroke Center) Signs and Symptoms of Hemorrhagic Transformation • neurologic worsening that may be sudden or progressive (depressed level of consciousness, sluggish pupillary response, headache, vomiting) • may be asymptomatic • possible motor or sensory changes • increasing blood pressure 5

Management • repeat CT scan to confirm diagnosis and direct further management • control blood pressure • avoid use of anticoagulants • surgery may be required (the majority of cases are non-surgical) • protect airway • monitor neurological and cardiovascular signs closely2. CEREBRAL EDEMA Cerebral edema occurs when the brain is deprived of oxygen as a consequence of a blocked cerebral artery. The blood-brain barrier breaks down which leads to an increase in the water content of brain cells and subsequent edema. Cerebral edema typically occurs in patients who have had an occlusion of the middle cerebral artery (MCA) and appears approximately 4 days after onset (AHA/ASA Guidelines for the Management of Adults with Ischemic Stroke, 2007). Signs and Symptoms of Cerebral Edema Early signs: • Decreased level of consciousness (LOC) (lethargy, talkative or quiet, restless or irritable, trouble remembering things) • Nausea and vomiting • Sluggish pupillary response to light Late signs: Signs of increased intra-cranial (ICP) pressure such as altered respiratory pattern, unequal pupils, fixed dilated pupils, decorticate or extensor posturing, loss of gag reflex, loss of corneal reflex and bradycardia. A late sign of increased ICP is Cushing’s triad: increased systolic blood pressure, widened pulse pressure, and slowed heart rate. Cushing’s triad develops when the patient’s brain can no longer compensate for the increase in pressure. Management • head of bed elevated to 30 degrees • proper positioning: maintain head in a midline position to assist venous drainage from the jugular veins • drainage of cerebrospinal fluid through extraventricular drain if required • administration of osmotic diuretics to decrease ICP 6

3. DYSPHAGIAWhat is Dysphagia? • Dysphagia is a delay or misdirection of food or fluid as it moves from the mouth to the stomach. • Dysphagia may occur when cerebral damage affects the cranial nerves. • Dysphagia involves swallowing difficulties caused by impaired coordination of the swallowing muscles, or limited sensation in the mouth or throat. Food or liquid may pass into the throat in an uncoordinated manner and enter the airway. • Dysphagia can cause blockage of the airway and pneumonia. It can lead to dehydration, weight loss, and malnutrition.Dysphagia occurs in about 55% of people with new onset strokes (Martino et al.,2005). Of those affected, approximately 50% do not recover to a normal swallow 6months after onset (Martino et al., 2000).Independent predictors of dysphagia include male gender, age greater than 70,disabling stroke, impaired pharyngeal response, incomplete oral clearance, andweakness or asymmetry of the palate (Mann & Hankey, 2001).Some individuals with dysphagia experience mild discomfort, while othersexperience complete inability to swallow. Dysphagia can arise at any of the fourstages of swallowing. • In the oral preparatory stage (under voluntary control), food and liquid are placed in the mouth. The lips and jaw close to seal the mouth. Saliva is produced. • In the oral propulsive stage (under voluntary control), food is chewed and formed into a ‘bolus,’ or clump. The tongue moves the bolus to the back of the mouth. • In the pharyngeal stage (involuntary), the food reaches the anterior faucial pillars at the back of the mouth. The swallow is triggered. The soft palate closes the nasopharynx. The larynx moves upward and closes to prevent any food or liquid from passing into the airway. Constrictors in the pharynx move the bolus towards the espophagus. The bolus then passes into the esophagus. 7

• In the esophageal stage (involuntary), the upper esophageal spincter relaxes. Peristalsis (a wave-like action) pushes the bolus through the lower esophageal sphincter and into the stomach. (Management of Dysphagia in Acute Stroke: An Educational Manual for the Dysphagia Screening Professional. Heart & Stroke Foundation of Ontario, 2006)Signs and Symptoms of Dysphagia: • Choking on food or liquid • Stifled, suppressed, or overt coughing during meals • Difficulty breathing • Nasal regurgitation • Moist, wet, hoarse, or ‘gurgly’ voice (change in voice quality) during meals • Complaints of food sticking in the throat • Drooling or loss of food from the mouth • Pocketing of food in cheeks • Slow, effortful eating • Delay in initiating the swallow • Difficulty swallowing pills • Avoiding food or fluids • Dehydration and malnutrition(Improving Recognition and Management of Dysphagia, Heart and StrokeFoundation of Ontario, 2002).**Dysphagia can be difficult to detect. Some patients may have ‘silentaspiration.’ They do not show any clinical signs of aspiration, such ascoughing or gagging. Screening for Dysphagia – TOR-BSST Patients should be screened for swallowing difficulties within the first 24 hours of admission after stroke. If patients are not alert, they should be monitored and screened when appropriate (Canadian Best Practice Guidelines for Stroke, 2013). The Toronto Bedside Swallowing Screening Test (TOR-BSST) is one type of a valid, reliable screening tool used to detect the possible presence of dysphagia. The TOR- BSST includes clinical indicators (a water test, tongue movement, and voice quality) that have been identified with the highest likelihood to predict dysphagia. (Martino, et al, in press). 8

Other tests listed in the Canadian Best Practice Guidelines for Stroke (2013) include the Standardized Swallowing Assessment, The Gugging Swallowing Screen (GUSS), The Acute Stroke Dysphagia Screen, The Emergency Physician Dysphagia Screen, The Modified Mann Assessment of Swallowing Ability (MMASA), and The MetroHealth Dysphagia Screen. Contact your regional stroke educator for training on administering tests such as the TOR-BSST. Management 1. Maintain patients NPO until a swallow test, such as TOR-BSST, has been performed. NPO prohibits the administration of oral medications, water, and ice chips. Medications could be administered by alternate methods such as through a naso-gastric tube or rectally. 2. Perform mouth care using a minimal amount of water to prevent colonization of bacteria before oral intake. Frequency: Minimum of twice daily. 3. Perform proper oral care after meals. This involves checking for, and clearing, any residue that may have ‘pocketed’ in the mouth. This also includes cleaning the mouth and tongue with a toothbrush to prevent colonization of bacteria. 4. Ensure that the family is aware of proper oral care techniques, including clearing the mouth with water prior to oral intake, clearing any residue after meals, and performing tooth brushing consistently after meals. 5. Consult a Dysphagia Therapist (Speech-Language Pathologist, Occupational Therapist, or Registered Dietician with appropriate training) for an assessment of patients with stroke presenting with features of dysphagia or pulmonary aspiration. 6. Consult a Dietitian or Dysphagia Team member to recommend an appropriate diet. 7. Consider initiation of enteral or parenteral feeds if the patient is unable to take PO fluids within 48 hours and consult a Dietitian for appropriate rate and solution. 8. Monitor patient for signs of dehydration.(APSS Inpatient Care and Rehabilitation and Community Reintegration Guidelines,2007) 9

When assisting the patient to eat: • ensure alertness and a calm environment • position patient upright at 90 degree angle to the seating plane and seat with head/chin slightly down • encourage patients to feed themselves whenever possible, to reduce the risk of pneumonia. • give one spoonful at a time (teaspoons only – never tablespoons) and remind patients to focus on swallowing, eat slowly and chew small bites carefully • keep patient upright for 30 minutes after eating • ensure that family is also aware of proper feeding techniques • assist in implementing any recommendations made by the speech- language pathologist, occupational therapist, or dietician (for example, different types of postures/positioning, or different food consistencies). (Improving Recognition and Management of Dysphagia, Heart and Stroke Foundation of Ontario, 2002). For a glossary of neurological terms, link to: http://www.strokecenter.org/education/glossary.htm 10

4. ASPIRATION PNEUMONIA Aspiration pneumonia refers to the abnormal entry of fluid, particulate substances or secretions into the airways. In the stroke population, aspiration is usually a sign of severe dysphagia - a major risk factor for the development of aspiration pneumonia. Three clinical syndromes comprise aspiration pneumonia: chemical pneumonitis, bacterial infection, and airway obstruction (Bartlett, J.G (2008). Aspiration pneumonia is most likely to occur in seriously affected stroke patients who are immobile and unable to cough. In addition to dysphagia, it may result from seizures, vomiting, prolonged recumbency, inability of patient to turn for feeding, utilization of naso-gastric tube or other invasive feeding device, or mechanical ventilation. The risk for developing pneumonia was found to be 7.6 times greater for those patients who aspirated compared to those who did not (Schmidt et al, 1994). Signs and Symptoms of Aspiration Pneumonia• Tachypnea• Tachycardia• Increased oxygen requirements• Fever• Wheezing• Crackles• Chills• Malaise (Courtesy of www.hawaii.edu)Prevention and Management1. Maintain patients NPO until a swallow screen as been performed. NPO prohibits the administration of oral medications, water and ice chips2. Perform mouth care, using a minimal amount of water, to prevent colonization of bacteria 11

3. Consult a SLP or appropriately trained specialist for an assessment of patients with stroke presenting with features of dysphagia or pulmonary aspiration 4. Protect airway and suction where appropriate 5. Prevent nausea and vomiting 6. Encourage patients to take deep breaths and/or use incentive spirometry to help lessen the potential for atelectasis 7. Consult attending physician or nurse practitioner for further management5. POST STROKE DEPRESSION (PSD) Some form of PSD has been found to occur in at least one-quarter of stroke survivors in the first year. One study found that approximately 33% of stroke survivors experience PSD. The majority of cases may develop in the first 3 months of stroke and incidence rates decline over time. Risk factors for PSD: • increasing stroke severity • functional dependence (requiring help with activities of daily living) • past history of depression • cognitive impairment It is unclear whether biochemical factors resulting from the stroke or secondary psychological responses to the physical, cognitive, and social impact of the stroke is the cause of post-stroke depression. There is wide diversity in studies that examined the relationship between the site of the brain lesion and depression. Not all studies have confirmed that a relationship exists and more research is required in this area. The impact of PSD includes the following: • increased risk of dependence • poorer function outcomes • poorer cognitive function • decreased participation in rehabilitation • reduced social participation • increased risk for mortality 12

Assessment of the post-stroke patient may be complicated bycognitive deficits that prevent the patient from recognizing orbeing able to report symptoms of depression. There is nosingle universally accepted tool for the assessment of PSD asmost tools were not designed for patients with cognitive and/orphysical impairments. An alternative to verbal scales used toassess mood should be sought when assessing someone whois aphasic, such as the Stroke Aphasia DepressionQuestionnaire.The Canadian Best Practice Recommendations for Stroke Care (2013)recommend that all patients with stroke be screened for depressive symptomsusing a validated tool at various stages throughout the continuum of stroke careand whenever the clinical presentation indicates. Stages may include: 1. during acute care stay, particularly if evidence of depression or mood changes 2. following hospital discharge from emergency department or inpatient setting to an outpatient or community based healthcare setting 3. throughout rehabilitation within inpatient, outpatient and home based settings, according to client progress 4. periodically following discharge to the community during follow-up appointments and/or during periodic health assessments with primary care practitioners and consulting specialists.Signs and Symptoms of Depression• persistent sad, anxious, feelings of hopelessness, pessimism, guilt, worthlessness, helplessness• loss of interest or pleasure in activities, decreased energy, difficulty concentrating, remembering, making decisions• insomnia, early-morning awakening or oversleeping• thoughts of death/suicide, suicide attempts• restlessness, irritability• withdrawal from activity, family, and friendsManagementPSD is frequently untreated because the symptoms of depression, includingsleep disturbance, decreased appetite, fatigue and feelings of hopelessness arecommon post-stroke symptoms. Patients screened as being at risk fordepression should be referred to a healthcare professional with expertise indiagnosis and management of depression in stroke.The following are strategies that may be used in the treatment of PSD:• May be initially managed by “Watchful waiting” if minor depression isdiagnosed (patient is monitored closely without additional therapeuticinterventions to determine whether symptoms will improve. Includes 13

suggestions to the patient for self-help strategies and participation in exercise) • Antidepressant medication (selective serotonin reuptake inhibitors-SSRIs) may be favored in this population • Psychotherapy (as an adjunct in combination with antidepressants)Other emerging approaches that require more research include: RepetitiveTranscranial Magnetic Stimulation (rTMs), cognitive behavioral therapy, Physicalexercise and acupuncture {Evidence level C}.Following initial treatment for PSD, patient should continue to be monitored forrecurrence of depressive symptoms. The involvement and feedback of family andcaregivers can be an important component of ongoing monitoring; Prevention of DepressionEarly attention by health care providers to social withdrawal or impaired socialfunctioning early on may help to deter depression and provide an opportunity forearly treatment and resumption of usual activities. Talk based interventions,including problem-solving therapy and motivational interviewing may be used toenhance rehabilitation and prevent depression post stroke. Engaging patients inactivities such as exercise or music therapy may also have a beneficial effect onmood post-stroke Reference: Canadian Best Practice Recommendations for Stroke Care (2013), Mood and Cognition in Stroke, recommendation 7.1: Identification and Management of Post-Stroke Depression (PSD)6. SEIZURES A seizure is a sudden change in behavior or physical findings that is a consequence of abnormal electrical activity in the brain. Stroke is the most common cause of seizures in the elderly population (Myint et al, 2006). It has been estimated that 11.5 % of patients with stroke are at risk of developing seizures within 5 years. Post-stroke seizures may be categorized as early seizures (occurring within 7 days after stroke) and late seizures (occurring beyond one week after stroke). Incidence varies with the underlying pathophysiology. Intracerebral haemorrhage is associated with the highest incidence of post‐stroke seizures (10.6%–15.4% of them develop the condition) and transient ischaemic attack is associated with the lowest incidence (3.7%) (Reuck et al, 2007; Feleppa et al, 2006). A cause of seizure activity after hemorrhagic stroke may be due to neuronal irritation caused by the products of blood metabolism. Late onset seizures may be a consequence of persistent changes in neuronal excitability and scarring. There have been several causes for early onset seizures after 14

ischaemic strokes postulated and accepted: a change in excitation propertiesinvolving intracellular Ca2+ and Na+, glutamate excitotoxicity, hypoxia, metabolicdysfunction, global hypoperfusion, and hyperperfusion injury (particularly aftercarotid endarterectomy).In ischaemic strokes, the severity of persistent disability after the stroke, theinvolvement of multiple sites or a larger lesion, and hippocampus involvementare factors that predict the likelihood of developing post‐stroke seizures.Another recognized risk for early post‐stroke seizures is embolic stroke (Myintet al. 2006)The following are also predictors of early seizure after an ischemic stroke:Hyperglycemia and/or hypoglycemia Hypernatremia and/or hyponatremiaHypocalcaemia HypomagnesaemiaRenal failure InfectionsAtrial fibrillation DiabetesCortical damage Hemorrhagic strokeSupratentorial infarcts Occipital atherothromobotic infarctionAcute confusion state Severity of initial stroke(Feleppa et al, 2006)In a study by Labovitz et al, (2001), NIHSS score was not found to be apredictor of early seizure after stroke.The presence of seizure at stroke onset is a relative contraindication forintravenous tPA as the concern is that tPA may be given to a patient withoutstroke (Sylaja et al, 2006). There is insufficient data on the efficacy ofanticonvulsants in the treatment of stroke patients who have experiencedseizures. Recommendations are based on current management of seizures(AHA/ASA Guidelines for the Early Management of Adults with IschemicStroke,2007).Signs of Seizure ActivityThe deficits that result as a consequence of stroke may complicate earlydetection of signs of seizure activity. Approximately 1/3 of patients present withgeneralized (tonic-clonic) seizures and the remainder present with partial(focal) seizures. Signs and symptoms of generalized seizures may include:loss of consciousness or fainting, general muscle contraction, rigidity, andrelaxation, biting the cheek or tongue, clenching teeth or jaw, incontinence,cessation or difficulty breathing during seizure, blue skin color. Signs andsymptoms of partial seizures may include: altered consciousness, abnormalmotor control and sensations, auditory or visual hallucinations, nausea,sweating, dilated pupils, possible memory loss of events occurring near thetime of the seizure. 15

Management • during a seizure protect patient from injury until seizure has passed • protect airway and suction as required • administration of antiepileptic agents should be selected by specific patient characteristics (ClassI; Level of Evidence B) (AHA/ASA Guidelines for the Early Management of Patients with Acute Ischemic Stroke, 2013) • document length of time of seizure activity and symptoms patient experiences during and after seizure • an electroencephalogram (EEG), CT or MRI may be required to identify the source of seizure activity7. VISUAL NEGLECT Visual neglect is defined as a failure to report, respond or orient to visual stimuli presented to the side opposite the brain lesion (Heilman, 1993). It is caused by cerebral injury resulting in a passive unconscious decreased awareness of part of the field of view or other stimuli to one side of the body. It usually occurs with a visual field defect, but may occur without loss of field. The Line Bisection Test is a validated and reliable screening test for visual neglect. This test requires the patient to cross through the midpoint of a series of lines. If 16

the patient is unable to do so, this may indicate the presence of visual neglect and need for further assessment.Signs of Visual Neglect • ignoring food on one side of the plate • attending to only one side of the body during activities of daily living • colliding into surrounding objects in environment Management Early detection of visual neglect prior to mobilization and/or promotion of self- care activities may optimize patient safety and prevent falls. It may be necessary to alter the environment to ensure the safety of the patient. Consider consultation by an OT to teach the patient to be aware of the neglected side.8. INCONTINENCE 8.1 Urinary Incontinence Urinary incontinence caused by stroke is due to afferent and efferent nerve dysfunction of bladder, sphincter, or pelvic floor muscles. Urinary incontinence affects 40% - 60% of people hospitalized with stroke and 15% remain incontinent after one year post-stroke (Woodward, 2013). The most common urologic dysfunction is detrusor hyperreflexia (Burney et al, 1996). This is caused by loss of inhibitory input from higher neurologic centers and results in an over-responsive, twitching, or spastic detrusor muscle. This leads to urgency, frequency, and urge incontinence (European Association of Urology (2006) Guidelines on Incontinence). Urinary incontinence may be categorized as follows: 1. Stress incontinence: may be due to poor bladder support by the pelvic muscles or to a weak or damaged sphincter resulting in urine leaking with activity that strains or stresses the abdomen, such as coughing, sneezing, laughing, or walking. 2. Urge incontinence: results when an overactive detrusor muscle contracts without voluntary intention, causing urine to leak without any warning. This is often associated with infection or decreased functioning of nerve fibers. 17

3. Overflow incontinence: occurs when the bladder muscles are inactive or the urethra is blocked and urine overflows, often in small amounts. Detrusor hyperreflexia occurs in most patients with frontoparietal and internal capsule infarcts while normal urinary function is likely to remain in patients with temporo-occipital lobe infarcts. Detrusor hyporeflexia and areflexia may also occur following stroke and lead to overflow incontinence. Bladder areflexia may occur with frontoparietal, internal capsule, basal ganglia, thalamic, pontine, and cerebellar infarcts (Burney et al, 1996).ManagementInterventions to Improve Continence: • Ensure adequate fluid intake • Assess post void residuals (PVR) (normal is less than 100 mLs of urine) • If available, use ultrasonic bladder scanner to check volume of urine in bladder following the void, checking for PVR prior to catheterization • Review medications (diuretics, anticholinergics) • Modify clothing to maintain hygiene • Introduce a regular toileting routine Q2-3H1. Interventions to Improve Storage: • Pelvic floor muscle training – Kegel exercises • Bladder training programs which increase the time interval between voids to increase bladder capacity over time. • Timed voiding which avoids incontinence episodes. • Pharmacological interventions – anti-muscarinics (Woodward, 2013).2. Interventions to Improve Emptying: • Indwelling catheterization not recommended as it promotes the development of a biofilm (a living layer of bacteria) on the catheter which promotes an urinary tract infection (UTI) • Intermittent catheterization recommended following bladder scan for PVR (Woodward, 2013) 8.2 BOWEL CONTINENCE • Constipation causes straining while having a bowel movement, resulting in increased intra-abdominal pressure and ICP which should be avoided (Hickey, 2009). • Bowel management program should be implemented in patients with persistent constipation or bowel incontinence (Lindsay et al., 2008; HSF, 2014).Management • Daily pelvic floor exercises • Use of suppositories (rather than laxatives) • Increased fluid intake (hydration) • Bulking agents rather than stool softeners (Harari et al., 2004). 18

9. URINARY TRACT INFECTIONS (UTIs) Urinary tract infections occur when microorganisms grow in the urine or structures of the urinary system. UTIs are relatively common among stroke patients but are most likely associated with severe strokes. Bacteremia or sepsis are potential serious complications of a UTI and may cause delirium to occur (AHA/ASA Guidelines for the Early Management of Ischemic Stroke (2007). A major cause of UTIs is urinary catheterization, which may be due to technique, method, duration, patient susceptibility, or type of set up (closed/open). Whenever possible, avoid the use of indwelling catheters. Signs and Symptoms of a UTI • Fever and chills • Nausea, vomiting & malaise • Frequency, urgency or burning when voiding • Urine may be cloudy, pink or bloody • Malodorous UTIs may be a cause of confusion (delirium) in older adults. To confirm diagnosis, consider collection for urinalysis and culture. Management • Consult attending physician or nurse practitioner • Maintain adequate hydration and nutrition • Administer prescribed antibiotics • Treat fever and pain • Monitor urine output for frequency, appearance and volume10. VENOUS THROMBOEMBOLISM (VTE) Venous thromboembolism includes deep vein thrombosis (DVT) and pulmonary embolus (PE). DVT is defined as a blood clot that forms in the veins of the lower limbs. A blood clot forms when cellular material, such as red and white blood cells and platelets become bound together by fibrin strands. DVT development may occur as early as the second day post-stroke, but has peak prevalence between 2 to 7 days post-stroke (Kelly et al, 2001). Diagnosis is aided by ultrasound.Symptomatic DVT slows recovery and rehabilitation after stroke. The risk of DVTis highest among immobilized and older patients with severe stroke. Patients withhemiparesis are predisposed to DVT development (Landi et al, 1992). 19

VenousCirculationSigns and Symptoms of DVT• Asymmetrical tenderness• Swelling• Warmth• Redness in lower extremitiesDVT may result in a pulmonary embolism (PE),which is a blood clot that obstructs blood flowin the pulmonary artery or any of its branchesA PE may occur without signs.Signs and Symptoms of PE• Sudden dyspnea• Tachypnea• Hemoptysis• Chest pain• Shock.Most patients who show clinical signs of PE require urgent investigation andpharmacological treatment (anticoagulation) if the diagnosis of PE is confirmed. High risk patients include: • Patients who are unable to move one or both lower limbs • Patients unable to mobilize independently • Patients who have a history of VTE • Dehydration • Comorbidities (eg. Cancer) (HSF, 2014).Management 1. If no contraindications: • Early mobilization • Maintain adequate hydration • Low molecular weight heparin or unfractionated heparin (for patients with renal failure) • Intermittent pneumatic stockings • Monitor for possible DVT and PE (HSF, 2014)2. If patient has had a systemic or intracranial hemorrhage: 20

• Early mobilization • Maintain adequate hydration • Antiplatelet and/or anticoagulant therapy should be avoided for at least 48 hours following bleed • Intermittent pneumatic compression (IPC) stockings • Monitor for possible DVT and PE (HSF, 2014) MOBILIZATION Defined as “the process of getting a patient to move in bed, sit up, stand and eventually walk” (HSF, 2014). • Early and frequent mobilization (within 24 hours of stroke onset unless otherwise contraindicated) • Assessed by rehabilitation professionals within 24-48 hours of admission, if possible (HSF, 2014).11.SHOULDER COMPLICATIONS 11.1 Shoulder Subluxation Shoulder subluxation is caused by a loss of muscle tone or flaccidity of the supporting shoulder girdle muscles after a stroke. This distorts the angulation of glenoid fossa downward. The humeral head is displaced inferiorly and/or forward. The downward pull of gravity on the unsupported arm contributes to overstretching the tendons, ligaments, and capsule. 11.2 Hemiparetic Shoulder Pain Pain associated with a hemiparetic shoulder can result in significant disability and may occur as early as two weeks post-stroke but is more commonly observed 2-3 months after. Causes of shoulder pain include:  Tendinopathies secondary to improper handling of the hemiparetic upper extremity as well as impingement (muscle imbalance secondary to changes in muscle tone)  Capsulitis and frozen shoulder  Complex Regional Pain Syndrome or Shoulder Hand Syndrome  Spasticity of the pectoralis and subscapularis muscles  Neurovascular compression (rarely) 21

Management of Shoulder Subluxation and Hemiparetic Shoulder Pain  avoid pulling/holding onto the hemiplegic arm to change position or to support the patient when sitting, walking or standing  avoid repositioning the patient in bed or wheelchair by lifting them under the arm  consult OT/PT for strategies to protect and provide support of the affected upper limb d u r i n g t r a n s f e r s a n d f u n c t i o n a l m o b i l i t y (i.e. u s i n g a s l i n g d u r i n g t h e f l a c c i d stage, wheelchair hemi tray or arm trough, w h e e l c h a i r lap tray, armrest padded with pillows, pocket of clothes in higher level patients)  daily gentle passive/self assisted movements in pain-free range  postural correction and education  administer analgesics, Botulinum toxin (Botox), or steroids as ordered  consult PT/OT or Physiatry for further management (Brender & McKenna, 2001)12. SPASTICITY Spasticity is a neurological condition causing an abnormal increase in muscle tone, stiffness, or tightness resulting in impaired movement. It occurs when muscles receive improper nerve signals causing them to contract. The degree of spasticity can vary from mild muscle stiffness to severe, painful, and uncontrollable muscle spasm and contracture. Signs and Symptoms of Spasticity A stroke patient with spasticity might be observed walking with an abnormal posture in which the arm is very tight and pulled up against the chest. A leg may be very stiff and swing out sideways. The patient may not be able to position a foot flat on the ground. Spasticity can be very painful if the joint is pulled into abnormal positions. A loss of range of motion at the affected joint, resulting in contracture may develop if therapy is delayed. Management • positioning, stretching and strengthening exercises as recommended by PT and OT • muscle relaxants • serial casting for contractures to allow tendons to stretch • local blocking agent, such as Botox, to block abnormal neuronal enervation of muscle tissue (Faast FAQS for Stroke Nurses, 3rd Ed, 2007) (Courtesy of Calgary Health Region) 22

13. CARDIAC COMPLICATIONS Cardiac complications are common after stroke. Pre-existing cardiac abnormalities are also highly prevalent among stroke patients. It is important to determine whether the cardiac abnormalities are caused by stroke, are the cause of stroke, or are unrelated to it. This section includes a brief description of normal physiology followed by major potential post-stroke cardiac complications. The following describes a normal ECG complex and waveforms:P wave • indicates atrial depolarization or contraction of the atrium • normal duration is not longer than 0.10 seconds (less than 3 small squares) • amplitude (height) is no more than 3 mm • rounded with no notching or peaking QRS complex • indicates ventricular depolarization or contraction of the ventricles • normally not longer than .12 seconds in duration • amplitude is not less than 5 mm in lead II or 9 mm in V3 and V4 • R waves are deflected positively and the Q and S waves are negative T wave • indicates ventricular repolarization • not more that 5 mm in amplitude in standard leads and 10 mm in precordial leads • rounded and asymmetrical • normally upright in I & V6, and inverted in aVR; they may invert in III, aVF, 23

aVL and V1 • V3, V4 or lead II optimize the T-waveU Waves • U waves are a small flat wave sometimes seen after the T wave and before the next P waveST segment • indicates early ventricular repolarization • normally not depressed more than 0.5 mm • may be elevated slightly in some leads (no more than 1 mm)PR interval • indicates AV conduction time • duration time is 0.12 to 0.20 secondsQT interval • measured from the beginning of the Q to the end of the T • represents ventricular depolarization and repolarization (sodium influx and potassium efflux) • QT usually less than half the R-R interval (0.32-0.40 seconds when rate is 65-90/minute) • QT varies with rate. Correct for rate by dividing QT by the square root of the RR interval. Normal corrected for rate is < 0.46 for women and < 0.45 for menCardiac abnormalities that are commonly associated with stroke are categorizedas follows: • repolarization and ECG abnormalities • dysrhythmias • elevated cardiac enzymes • myocardial infarction • neurogenic cardiac damage 13.1 Repolarization and ECG AbnormalitiesRepolarization abnormalities increase the period of time when prematureconduction/ extrasystoles may result in ventricular tachycardia or fibrillation(R onT phenomenon). Large upright T waves and prolonged QT intervals may occur inpatients with subarachnoid hemorrhage, ischemic stroke, and TIAs. (Hachinski,1993; Korpelainen et al, 1997).Large T waves have been noted in 50% of patients with intracranial hemorrhageand are common following left frontal hemorrhage (Byer et al, 1947). 24

QT prolongation is the most common stroke-related ECG abnormality and isfound in 71% of patients with subarachnoid hemorrhage, 64% of patients withintraparenchymal hemorrhage, and 38% of patients with ischemic stroke Yamouret al, 1980).For patients with subarachnoid hemorrhage, serious ventricular dysrhythmias,including sudden death and polymorphic ventricular tachycardia (ie. torsadesde pointes are often preceded by QT prolongation. QT prolongation may occurmore commonly with right rather than left hemispheric stroke (Oppenheimer etal, 1995; Hachinski et al,1992).ST segment changes are generally transient and may r e p r e s e n t myocardialischemia or infarction (Oppenheimer et al, 1995).Abnormal Q waves are >0.04 seconds and >25% of the height of the following Rwave. Q waves are often seen after acute stroke (Goldstein, 1979; Lavy et al,1974; Samuels, 1984). They may be transient or evolve in a similar fashion seenafter myocardial infarction.The presence of U waves may be seen with hypokalemia but are common afterstroke in the absence of any electrolyte abnormality (Samuels, 1984). 13.2 DysrhythmiasThe most common post-stroke dysrhythmias are ventricular extra systoles,supraventricular tachycardia, and atrial fibrillation (Rem et al, 1985). Lead II - Atrial fibrillationOf the preceding dysrhythmias, only ventricular dysrhythmias have beenassociated with increased mortality after stroke. Atrial fibrillation is an importantpotential cause of stroke due to the potential for development of emboli. Itsdiagnosis if often challenging if it is proxsymal. Treatment for atrial fibrillationincludes the use of ASA, warfarin, direct thrombin inhibitor or a direct factor Xainhibitor. Introduction of warfarin, direct thrombin inhibitor or a direct factor Xainhibitor in the case of acute ischemic stroke may be delayed due to potential riskof hemorrhagic transformation if introduced immediately. Warfarin may beintroduced 7-10 days after an ischemic stroke and once a CT of the brain rulesout hemorrhage. The initiation of a direct thrombin inhibitor must be done withcare as its anticoagulation effects are established more quickly than Warfarin.Bradycardia may be more common with injury of the right insula, whiletachycardia and hypertension may be more common with injury of the left insular 25

region. Supraventricular dysrhythmias are more common after right than lefthemisphere stroke. The cause may be due to impaired parasympathetic tonecaused by right hemispheric injury (Hachinski et al, 1992; Lane et al, 1992). 13.3 Elevated Cardiac EnzymesTroponin levels may be useful in differentiating neurogenic left ventriculardysfunction associated with subarachnoid hemorrhage from dysfunction causedby myocardial infarction. Cardiac markers are frequently elevated in acuteischemic stroke occurring in 5-34% of patients. These elevations haveprognostic implications where elevations in Troponin I are associated withincreased stroke severity and mortality risk (Some studies suggest that there arelower levels of troponin elevation associated with reversible myocardialdysfunction from stroke than with a myocardial infarction. Elevation of troponinsand other cardiac enzymes after acute stroke may also be related to stroke-related autonomic dysfunction. 13.4 Myocardial InfarctionCoincident stroke and myocardial infarction are common findings. Acutemyocardial infarction may lead to stroke and vice versa. Treatment options forischemic stroke are limited when occurring with recent myocardial infarction.Myocardial infarction occurring in the previous 3 months is a relativecontraindication for thrombolysis in acute stroke (AHA/ASA Guidelines for theEarly Management of Patients with Acute Ischemic Stroke, 2013). 13.5 Neurogenic Cardiac DamageEvidence of subendocardial infarction or anterolateral ischemia (i.e. ST segmentchanges or enzyme elevation) is common after stroke, particularly in the case ofsubarachnoid hemorrhage. Myocardial injury may be the result of a centrallymediated release of catecholamines due to hypoperfusion of the posteriorhypothalamus (Oppenheimer et al, 1995; Chua et al, 1999).Signs and Symptoms of Cardiac Complications • worsening of cardiovascular status (alterations in blood pressure, heart rate or rhythm, diminishing peripheral pulses, cyanosis) • chest, back, shoulder, or neck pain • shortness of breath, tachypnea, dyspnea • signs of pulmonary edema (decreased air entry to lungs, cough, frothy sputum) • diaphoresis, pallor, vomiting • dizziness, decreased mentation, headache, loss of consciousness • ECG changes 26

Management • all stroke patients should receive a clinical cardiovascular examination, cardiac enzyme tests, and a 12 lead ECG (AHA/ASA Guidelines for the Early Management of Ischemic Stroke, 2007) • patients who received tPA require cardiac monitoring for a minimum of 24 hours (APSS Inpatient Care for Acute Stroke Admissions Recommendations, 2009) • arrange for echocardiography to rule out a possible cardiac source of emboli as cause of ischemic stroke. Note:Transesophageal echocardiogram is the gold standard to rule out thrombus in the left atrial appendage) • monitor cardiac enzymes (Troponin I; and for prognostication Troponin T) • monitor electrolyte levels • assess for potential adverse effects of medications and potential drug- drug interactions (i.e. beta blockers, calcium channel blockers, anti- arrhythmics, inotropes, and QT prolonging medications such as phenothiazines and tricyclic anti-depresssants) • treat dysrhythmias when indicated • consult physician immediately if changes in neurological and cardiovascular status occurCongratulations! You have completed this learning module!A table for quick reference and a set of study questions with an answer key follows.Please provide feedback on this learning module by completing the Participant Evaluation Form. 27

Preventing Complications of Stroke Quick Reference TableHemorrhagic Etiology Signs & Symptoms ManagementTransformation There may be NO  Urgent CT Ischemic tissue signs or symptoms.  Control BPCerebral Edema becomes injured &  Avoid fragile. When blood Headache, vomiting,Dysphagia flow is restored, the depressed LOC, anticoagulants injured tissue worsening neurologic  Possible surgicalAspiration becomes leaky signs, increasing BP,Pneumonia allowing blood to motor or sensory removal of clot seep into surrounding changes  Protect airway tissue  Close neurological Brain tissue becomes Worsening & cardiovascular ischemic which leads neurological signs, to breakdown of depressed LOC, monitoring blood-brain barrier. headache, dizziness,  Head of bed Water content of vomiting, possible cerebral cells widening of pulse elevated to 30 increases causing pressure, cerebral edema bradycardia, degrees respiratory changes  Head in midline Cerebral damage Choking on food, position resulting in impaired frequent or impaired  Drainage of enervation of cranial cough, nasal nerves V, VII, IX, X, regurgitation, wet cerebral spinal fluid XII. Results in voice, c/o difficulty  Administer osmotic impaired coordination swallowing food or of the swallowing pills, drooling, diuretics to ↓ICP muscles or limits pocketing food in  Close neurological sensation in the cheeks, delay in mouth and throat initiating swallow, & cardiovascular signs of aspiration (coughing, choking, monitoring respiratory distress)  Consult Dysphagia, seizures, Tachypnea, SLP/Dyshagia vomiting, prolonged tachycardia, fever, recumbency or wheezing, crackles, Team and Dietician mechanical chills, malaise, c/o  Maintain NPO until ventilation resulting in SOB aspiration of food or swallow screen secretions, inability to turn or position for performed feeding, placement of  Perform mouth care naso-gastric tube or other invasive with minimal water feeding devices  Consider enteral or parenteral feeds if unable to take fluids within 48 hours  Monitor for signs of dehydration  Maintain NPO until swallow screen  Perform mouth care  Consult SLP/Dysphagia Team  Protect airway  Maintain oxygenation  Prevent nausea and vomiting  Administer 28

Post-Stroke Unclear-may be Persistent sad, antibiotics ifDepression biochemical factors anxious, feelings of indicated resulting from stroke hopelessness,  Encourage deepSeizures or psychological pessimism, guilt, breathing responses to the worthlessness,  Attend to earlyVisual Neglect physical, cognitive, or helplessness, loss of signs of social social impact of interest or pleasure in withdrawal orContinence Care stroke activities, decreased impaired social(Urinary and Bowel) energy, difficulty functioning Damage to cerebral concentrating,  Assess using tissue causing remembering, making validated neuronal dysfunction, decisions, insomnia, assessment tool irritability, and/or early-morning  Administer anti- excitability awakening or depressants oversleeping,  Consult Cerebral injury thoughts of Psychologist causing a passive death/suicide, suicide  Provide emotional unconscious attempts, support decreased restlessness, awareness of part of irritability, withdrawal  Protect patient from the field of view or from activity, family, injury until seizure other stimuli to one and friends has passed side of the body. It Signs of generalized usually occurs with a or partial seizure  Protect/maintain visual field defect, but activity (may include airway, suction as may occur without loss of or altered required loss of field consciousness, Afferent and efferent muscle contraction  Administer anti- nerve dysfunction of and rigidity, convulsants bladder, sphincter, or incontinence, pelvic floor muscles; cessation or difficulty  Document length of blockage of urethra, breathing, memory time of seizures and UTI loss) symptoms (pre & post seizure) Patient collides into surrounding objects,  Alter the ignores food one side environment to of the plate, or ensure safety of attends to only one patient side of the body for hygiene  Teach the patient to be aware of the Urgency, frequency, neglected side often leaking, nocturia through occupational therapy  Consult OT  Variable  May involve intermittent catheterization  Teach Kegel exercises 29

UTI Growth of Fever, chills, nausea,  Ensure adequate microorganisms in vomiting, malaise,VTE (includes both urine of urinary frequency, urgency, fluid intakeDVT and PE) structures - major burning when  Assess post-void cause is urinary voiding, cloudy, pink,Shoulder catheterization bloody or malodorous residualsComplications urine. May cause  Treat UTI if present Blood cells bind with elderly patients to  Bladder re-trainingSpasticity fibrin strands to form become confused.  Regular toileting a blood clot in the May beCardiac veins of the lower asymptomatic routinecomplications limbs – major cause  Bowel is immobility Asymmetrical tenderness, swelling, management Compression of warmth, and redness neurovascular in lower limbs program structures between Pain, inappropriate  Maintain hydration the clavicle and lst alignment and ROM rib, pectoral muscles of upper limbs and nutrition and 3rd, 4th, & 5th ribs  Avoid use of resulting in postural Abnormal posture or changes and lack of gait, improper indwelling catheters trunk muscle control positioning of arm against chest, leg if possible Improper neuronal stiffness, difficulty  Administer enervation causing placing foot flat on abnormal increase in the round antibiotics muscle tone and  Treat fever and pain stiffness with potential for  Ambulation asap contractures  Maintain hydration  Elevate legs  Administer anticoagulants if not contraindicated  Monitor for PE  Postural correction and positioning  ROM exercises  Support affected arm  Administer analgesics, Botox, steroids as ordered  Consult PT, Physiatry OT  Position limbs appropriately  Consult PT or OT  Administer muscle relaxants or Botox as ordered  Serial casting for contractures Variable-cardiac Worsening of  Neurological and dysfunction may cardiovascular status; occur concurrently chest, back, cardiovascular with stroke; centrally shoulder, or neck mediated release of pain; shortness of monitoring catecholamines due breath, tachypnea,  Cardiac monitoring to hypoperfusion of dyspnea; signs of posterior pulmonary edema; for at least 24 hours hypothalamus; diaphoresis, pallor, lesions in portions of vomiting, dizziness, post tPA cerebral hemisphere decreased mentation,  Monitor cardiac influencing cardiac headache, LOC, function and ECG changes enzymes  Arrange for echocardiogram if possible cardiac source of emboli  Monitor electrolyte3s0

autonomic regulation  Review medications  Treat dysrhythmias when indicated  Consult physician immediately if changes in neurological and cardiovascular status occur 31

Review Questions:1. Which 2 statements are true regarding hemorrhagic transformation?a. It is a complication of ischemic stroke that usually occurs within 1-2 daysb. It is a complication of hemorrhagic stroke that usually occurs within 1-2 hoursc. It occurs when cerebral arteries spontaneously rupture as a result of an embolusd. It occurs when cerebral blood flow is restored to injured blood vessels2. The following are signs of hemorrhagic transformation, except:a. Hypotensionb. Headachec. Depressed level of consciousnessd. Vomiting3. Which statement with respect to cerebral edema is false?a. Treatment involves administration of anticoagulantsb. Likelihood of occurrence is highest 4 days after an ischemic eventc. It occurs when the water content of brain cells increasesd. May be treated with osmotic diuretics4. Which statement is not true regarding dysphagia?a. It is defined by the inability to swallow solidsb. It may result in airway obstruction or aspiration pneumoniac. Signs include choking, wet voice, coughing during meals, or no signs at all.d. Patients should be kept NPO until a swallow screen is performed5. Assisting a patient to eat involves the following, except:a. Positioning patient upright at 45 degrees to the seating planeb. Performing mouth care before and after oral intakec. Remaining upright for 30 minutes post-feedingd. Giving one teaspoonful at a time6. You are trained to administer the TOR-BSST. After administering it to oneof your patients, you suspect that the patient is aspirating. You talk to one ofthe following team members about your concern:a. SLP or OT onlyb. OT or PT onlyc. SLP, OT, RD, or another, appropriately trained, dysphagia cliniciand. SLP, PT, RD, or another, appropriately trained, dysphagia clinician 32

7. Assisting a patient to eat involves the following, except: a. Positioning patient upright at 45 degrees to the seating plane b. Performing mouth care before oral intake c. Remaining upright for 30 minutes post feeding d. Giving one teaspoonful at a time 8. Which statement regarding post-stroke depression is false? a. The time for greatest risk is within the first 6 months post-stroke b. Risk factors include female sex, social isolation and functional impairment c. The site of lesion can help predict the likelihood of developing post- stroke depression d. Signs and symptoms include loss of interest or pleasure, insomnia, restlessness or irritability 9. Which statement regarding post-stroke depression is false? a. All patients should be screened for depression at transition points b. SSRIs are used to treat depression c. Patients with post-stroke depression are less likely to utilize health care resources d. Post-stroke depression may be left untreated because symptoms may be similar to common post-stroke symptoms 10. Depression in aphasic stroke patients by may be assessed using this tool:11. Which statement is true regarding spasticity? a. A neurologic condition causing an abnormal decrease in muscle tone b. A musculoskeletal condition resulting in flaccidity and improper movement c. A consequence of stroke that results in the improper conduction of nerve signals to muscles d. It untreated, may result in abnormal lengthening of joints 12. Signs of visual neglect are all of the following except: a. Ignoring food on one side of the plate b. Colliding into surrounding objects when ambulating c. Forgetting location of car keys d. Attending to only one side of the body when bathing 33

13. Patients with stroke caused by an intracerebral hematoma are at higher risk of seizure than those with an ischemic stroke. True or False? 14. The following statements regarding urinary incontinence in stroke patients are true, except: a. Caused by afferent and efferent nerve dysfunction b. The most common post-stroke symptoms are frequency, urgency, and burning when voiding c. Overflow incontinence may occur when the urethra is blocked and urine leaks out d. Urinary incontinence affects 40% - 60% of people hospitalized initially with stroke and about 15% remain incontinent after one year. 15. Management strategies for urinary incontinence may involve 2 of the following strategies: a. Timed voiding to avoid incontinence episodes b. Administration of diuretics c. Assessment of post-void residuals d. Fluid restriction 16. A major cause of UTIs is the prolonged use of indwelling catheters. True or False? 17. The following statements regarding UTIs are true, except: a. Signs and symptoms are fever, chills, vomiting, frequency, and urgency b. UTIs may be a source of confusion in older adults c. Urine may appear cloudy, pink or malodorous d. Resolve over time and require no treatmen18. The following statements regarding bowel continence are true except: a. Constipation causes straining while having a bowel movement which can result in increased intra-abdominal pressure and ICP and should be avoided. b. Daily pelvic floor exercises (Kegel exercises) c. Fluid restriction to manage constipation d. Bowel management program should be implemented in patients with persistent constipation or bowel incontinence. 34

19. Which statement regarding VTE is false? a. Formed from blood cells bound by fibrin strands in the lower limbs; b. Diagnosis is aided by ultrasound c. Maintain bedrest as a treatment d. May result in a pulmonary embolism20. VTE can be prevented by the following, except: a. Bedrest to prevent mobilization of the clot b. Maintenance of adequate hydration c. Antiplatelet and/or anticoagulant therapy is recommended when there is no complications d. Early mobilization21. List four signs of a pulmonary embolism: , ,22. Hemiparetic shoulder pain is caused by all of the following, except:a. Improper handling of the hemiparetic upper extremityb. Capsulitis and frozen shoulderc. Spasticity of the pectoralis and subscapularis musclesd. Positioning the hand in contact with a surface23. Which statement regarding aspiration pneumonia is false?a. It may result from dysphagiab. It can be prevented by treating nausea and vomitingc. It is caused by deep breathing exercisesd. It has a high mortality rate24. List four signs or symptoms of aspiration pneumonia: , ,25. Ventricular dysrhythmias are associated with increased mortality after stroke.True or False?26. Supraventricular dysrhythmias are more common after right hemispheric stroke due to the following:a. Impaired parasympathetic tone 35

b. Increased likelihood of QT prolongation c. Development of U waves d. Increased likelihood of ST segment elevation27. Which statement is false? a. QT prolongation is the most common stroke-related ECG abnormality b. QT prolongation is a common finding in patients with subarachnoid hemorrhage c. QT prolongation may precede torsades de pointes in patients with subarachnoid hemorrhage d. The presence of a prolonged QT interval is associated with elevated cardiac enzymes 36

PREVENTING COMPLICATIONS OF STROKE Answer Key1. a & d2. a3. a4. a5. a6. c7. a8. c9. c10. Stroke Aphasia Questionnaire11. c12. c13. True14. b15. a & c16. True17. d18. c19. c20. a21. sudden dyspnea, tachypnea, chest pain, shock, hemoptysis22. d23. c24. tachypnea, tachycardia, fever, wheezing, crackles, chills, or malaise25. True26. a27. d 37

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