Presentation on theme: "TIA/CVA & NEUROLOGICAL ASSESSMENT 2015"— Presentation transcript:
1TIA/CVA & NEUROLOGICAL ASSESSMENT 2015 Ida Shepherd.Many neurological disorders occur for reasons beyond our control, but some can be prevented or minimised.
2Learning Outcomes Define various neurological conditions Identify risk factors for strokeDescribe the functions of each of the 4 brain lobesList the mechanisms of ischaemic cell injuryDifferentiate between subarachnoid and intracerebral haemorrhagic strokesDescribe the pathology of TIA’sCompare & contrast 5 types of CVAIdentify the physiological/cognitive effects of a CVADescribe the nursing interventions for patients experiencing a CVA or post-CVADescribe the basic principles of nursing care of a patient with IICP.Identify how to care for a seizure patient.Demonstrate the principles of a basic neuro assessmentTo appreciate the significant changes that take place with aging, a brief review of the neurologic system is required.
3Significant changes in aging nervous system The central nervous system (CNS) is divided into three major functional components: higher level brain or cerebral cortex, lower level brain (basal ganglia, thalamus, hypothalamus, brainstem, and cerebellum), and spinal cord.The brain is divided into three major areas, which include the cerebrum, brainstem, and cerebellum.
4DefinitionsCerebrovascular disease refers to any pathological processes involving the blood vessels of the brain.Cerebrovascular accident (CVA) – a focal neurological dysfunction whose symptoms last over 24 hours.Brain Attack – a term for CVA/Stroke.Transient Ischaemic Attack (TIA) – a brief episode of neurological deficit that resolves without any residual effect.All conditions require immediate attention - time is of the essence
5DefintionsReversible Ischemic Neurological deficit (RIND) – a neurological deficit persisting beyond 24 hours but resolving with no permanent deficit.Stroke – a generic term, lacking pathological meaning & laypersons term.Stroke in evolution- Progressive neurologic deterioration occurs; residual neurologic deficit present. Develops over 1-3 daysCompleted Stroke-Patient appears stable with neurologic deficit permanent and unchanging
6EpidemiologyCerebrovascular disease was the third leading cause of death in the total population in 2006, after cancer and ischaemic heart disease.There were 2674 deaths from cerebrovascular disease in 2006 and the majority (62.6 percent) were female deaths.Māori females had the highest age-standardised mortality rate of the four groups in 2006, followed by Māori males. The calculated Māori male age- standardised rate was 6.6 percent higher than the non-Māori male rate in 2006, and the calculated Māori female rate was 34.3 percent higher than the non-Māori female rate.
7Stroke Foundation Facts Stroke is the third largest killer in New Zealand (about 2500 people every year). Around 10 percent of stroke deaths occur in people under 65.Every day about 24 New Zealanders have a stroke. A quarter occur in people under 65. To recognise a stroke click here.Stroke is the major cause of serious adult disability in New Zealand.Stroke is largely preventable, yet about 9000 New Zealanders every year have a stroke. For information about reducing your stroke risk click here.There are an estimated 60,000 stroke survivors in New Zealand. Many are disabled and need significant daily support. However, stroke recovery can continue throughout life.Most people can’t recognise the signs of a stroke occurring. Make sure you are aware of the signs to look for. For more information click here.High blood pressure is a major cause of strokes. One in five New Zealanders has high blood pressure, and a third of these don’t know it. Reducing your blood pressure can greatly reduce stroke risk. For more information click here.Stroke is a medical emergency but many New Zealanders do not have access to the best possible stroke hospital services.http//www.stroke.org.nz/media/htmStroke affects annually around 17 million people globally
8EpidemiologyStroke is the second most common cause of death worldwide and a common cause of disability in adults in developed countries (Johnston et al, 2009; Rothwell, 2001).Stroke is a major public health challenge in New Zealand (MOH, 2000). It is the third greatest cause of death in New Zealand, after all cancers combined and heart disease (MOH, 2009), and has an enormous physical, psychological and financial impact on patients, families, the health care system and society (Strong et al, 2007; Caro et al, 2000).A systematic review of 56 stroke incidence studies (Feigin et al, 2009) showed that the age-adjusted stroke incidence rate in New Zealand is high compared with other developed countries.Approximately 6000 New Zealanders suffer from a stroke every year (Brown, 2009; Tobias et al, 2007) and approximately 2000 deaths each year are attributable to stroke
9EpidemiologySignificant disparities exist between Māori and non-Māori in the prevalence of stroke risk factors, stroke incidence and mortality rates, access to stroke care and stroke outcomes. Māori are also younger on average at first stroke onset than New Zealand Europeans (mean age 61 years compared with 76 years).
10EpidemiologyPacific peoples, along with Māori, experience strokes at high rates compared with other New Zealanders.Pacific stroke mortality rate for 2001 to 2004 was over two times the mortality rate of European/Other New Zealanders for the same period (Blakely et al, 2007).In 2001 to 2004, age-standardised stroke mortality rates were 27.3 per 100,000 for Pacific males and 19.9 per 100,000 for Pacific females. There was no significant difference in these stroke mortality rates between males and females (Blakely et al, 2007).Studies on the incidence of stroke show onset occurring at younger ages among Pacific people (Anderson et al, 2005; Bonita et al, 1997b; Carter et al, 2006; Feigin et al, 2007; Fink, 2006) and on average, 10 to 15 years earlier compared with New Zealand Europeans (Carter et al, 2006).This higher incidence of stroke among Pacific people is associated with the presence of more risk factors for stroke including diabetes, obesity, smoking and hypertension (Carter et al, 2006; Fink, 2006; Feigin et al, 2006), and may also reflect lower use of primary and secondary preventive care (eg, lower use of cholesterol- lowering and blood pressure control medications) (Fink, 2006).In addition Pacific peoples, along with Māori and Asian/Other New Zealanders, experience more severe strokes than New Zealand Europeans (CTRU, 2010).
11Risk factors Age Oral contraceptive use (especially if a smoker) Male Heart Disease & AFDiabetes↑ hematocrit or other hypercoagulability statesEarlier stroke or TIAAsymptomatic carotid artery stenosisHypertensionOral contraceptive use (especially if a smoker)Family historyExcessive ETOH intakeDrug abuseObesitySedentary lifestyleElevated serum cholesterol & triglyceridesMigrainesCigarette smokingSickle cell disease
12Revision- Physiology of the brain Major arteries supplying the brain Carotids supply anterior portion of brain. Vertebral - basilar artery and supplies the posterior portions of the brain.
13The Circle of Willis - In theory allows blood to circulate from one hemisphere to other - Functionally, two hemispheres usually remain separatePicture 43-2 p. 1365The circle of Willis is the region of the brain in which the branches of the basilar and internal carotid arteries join, creating a circular network, which in theory allows blood to circulate from one hemisphere to the other and from the anterior to the posterior portions of the brain.The Circle of Willis has a downside, however.Cerebral aneurysms tend to occur at the junctions between the arteries that make up the CircleCollateral circulation - an alternative route
14Cerebral Cortex and Functions Revise all own notes from Patho & A & PTexts: Lewis & Jarvis
15CPP is measured by monitoring ICP Optimal Cerebral Perfusion Pressure (CPP) has a MAP of 50mmHg which is maintained with mL of blood /min, using 20% of the CO.When perfusion falls below 50mmHg, cerebral ischaemia begins (syncope/ blurred vision) & cerebral vessels dilate & constrict in response to changes in BP & CO2 retention.A complex cascade of biochemical changes occur in response to the ischemia
16Ischaemic Cell InjuryInterruption of oxygenated blood flow to an area of the tissue (heart, brain, limb) (cerebral blood flow falls to less than 25mL/100g/min)Oxygen tension within cell decreases leading to decreased ATPLocal acidosis build-up, pH levels changeFailure of sodium pump, decreased potassiumInflux of sodium and water into cell causing swellingProgressive loss of glycogen and protein synthesisMorphologic deterioration (cell structure begins to degenerate)Mitochondria begin to swell, EPR dilatesGlutamate released causing further cell damageReversible to this point with reperfusion of tissuesDo some more reading around this partic after irreversibilityThe brain is very sensitive to a decrease in blood supply. As a result, when cerebral blood flow is reduced to a level insufficient to maintain neuronal viability, it causes a state of hypoxia. This hypoxic state leads to tissue ischemia and injury. Short-term ischemias result in TIAs. Long-term ischemia leads to permanent infarction (death of cerebral cells).(Meiner, Sue E.. Gerontologic Nursing, 3rd Edition. Mosby, ).
18CT scan taken some time after a large stroke CT scan taken some time after a large stroke. The black area is where the stroke was and now the brain tissue has died and left a large hole.
19Transient Ischaemic Attacks (TIA’s) Results from temporary impairment of blood flow to a specific region of the brain due to atherosclerosis, obstruction of cerebral microcirculation by a microembolus, a decrease in CPP (N=50mmHg) or cardiac arrhythmias.TIA’s can’t be distinguished from a stroke, but before diagnosing TIA consider other cases of transient neurological dysfunction – migraine, partial seizures, hyper/hypoglycaemia, hypotension, syncopePost TIA, 5-10% of patients will develop infarction if left untreated. Risk greatest in the first 7 weeks.Not all patients who develop cerebral infarction have had a warning TIA.ABCD 7 Day Stroke Risk ScorecardIf flow is restored within the critical period, ischaemic symptoms will reverse themselves.The ABCD score can be used in routine clinical practice to identify high-risk individuals who need emergency investigation and treatment.
20Aetiology - CVAIschemic stroke results from complete or partial occlusion of one or more cerebral blood vessels secondary to thrombus formation (site of stenosis as seen in atherosclerosis) or embolisation (resulting from an embolus commonly originating in the heart, may be due to AF). Cerebral oedema develops within minutes of the insult to the neuronal cells, peaks within 2 to 4 days, and contributes to neurolgic deficits.
21Ischaemic Strokes-80-85% Large artery thrombotic strokes: Due to atherosclerotic plaques in the large blood vessels of the brain. Thrombus formation and occlusion at the site of the atherosclerosis result in ischaemia and infarction.Small penetrating artery thrombotic strokes:Affect one or more vessels and are the most common type of ischaemic stoke. These are also called lacunar strokes because of the cavity that is created once the infarcted brain tissue disintegrates.Cardiogenic embolic strokes:Are associated with cardiac arrhythmias, usually atrial fibrillation. Emboli originate from the heart and circulate to the cerebral vasculature, most commonly the left middle cerebral artery, resulting in a stroke. Embolic strokes may be prevented by the use of anticoagulation therapy in patient with atrial fibrillation.Cryptogenic Strokes:Have no known cause; idiopathic.Other strokes:From causes such as cocaine use, coagulopathies, migraine, and spontaneous dissection of the carotid or vertebral arteries.Information from: Farrell (2004), p. 1896Percentages from: The University Hospital, Newark, New Jerseyhttp://www.theuniversityhospital.com/stroke/rehab.htm
22Haemorrhagic Strokes- 15-20% Typically classified by location of bleeding Subarachnoid haemorrhagic stroke- bleeding into subarachnoid space.- usually rupture of cerebral aneurysm or arteriovenous malformationIntracerebral haemorrhagic stroke- occurs from bleeding into brain tissue itself.- rupture of a small artery – often deep penetrating vessel, & often related to poorly controlled hypertension.Abrupt increase in intracranial pressure (ICP) which may cause cerebral oedema(With intra cerebral bleeding blood is forced into the adjacent brain tissue then extends the ischaemic damage – can result in brain tissue displacement or herniation)Subarachnoid haemorrhage causes:Sacular (Berry aneurysm)FusiformIntracerebral haemorrhage causes:High blood pressure (hypertension) is the most common cause of this type of stroke.Blood Vessel Abnormalities: Blood vessel abnormalities in the brain include arteriovenous malformations (AVMs) and arteriovenous fistulas (AVFs).
2310 percent of stroke survivors recover almost completely 25 percent recover with minor impairments40 percent experience moderate to severe impairments requiring special care10 percent require care in a nursing home or other long-term care facility15 percent die shortly after the stroke
27Herniation of the brain & Intracranial Pressure When the intracranial pressure increases enough it will cause particular regions of the brain to herniate into adjacent compartments, resulting in mechanical and secondary vascular damage.Cushing’s response is seen when cerebral blood flow decreases significantly: elevated SBP, widening pulse pressure and decreased HRFollowing this, the patient will exhibit significant changes in mental status and vital signs and Cushing’s triad appears: bradycardia, hypertension and bradypnoea.As ICP continues to rise, restlessness, confusion or increasing drowsiness may appear followed by the patient becoming stuperous.
28Care of the patient with IICP Alteration in LOC ranging from irritability, restlessness, and confusion to lethargyPossible onset or worsening of headacheBeginning pupillary dysfunction, such as sluggishness; visual disturbances, such as diplopia or blurred visionOnset of or increase in sensorimotor changes or deficits, such as weaknes;Onset or worsening of nausea.Continued deterioration of LOC leading to stupor and coma; projectile vomitingHemiplegia; posturingAlterations in VS (typically increased SBP, widening pulse pressure, decreased pulse rate); respiratory irregularities, such as Cheyne-Stokes breathing; pupillary changes, such as inequality, dilation, and non-reactivity to light; papilledemaImpaired brainstem reflexes (corneal, gag, swallowing).Early indicators of IICPLate indicators of IICP
29Increased intracranial pressure can be due to a rise in cerebrospinal fluid pressure. It can also be due to increased pressure within the brain matter caused by a mass (such as a tumor), bleeding into the brain or fluid around the brain, or swelling within the brain matter itself.Brain herniation: Occurs when IICP causes displacement of brain tissue from one intracranial compartment to another, resulting in compression, destruction, and laceration of brain tissue.In the presence of actual brain herniation, patient is in a deep coma, pupils become fixed and dilated bilaterally, posturing may progress to bilateral flaccidity, brainstem reflexes generally are lost, and respirations and VS deteriorate and may cease.
30The single most important early indicator of IICP is a change in LOC The single most important early indicator of IICP is a change in LOC. Late indicators of IICP usually signal impending or occurring brainstem herniation.Signs generally are related to brainstem compression and disruption of cranial nerves and vital centres. Hypotension and tachycardia in the absence of explainable causes, such as hypovolemia, usually are seen as a terminal event in TBI.IICP usually peaks around 72 hr after initial insult and then gradually subsides over 2–3 wk.
31Cushing’s Triad Bradycardia Hypertension Bradypnoea Cushing's triad is a clinical triad variably defined as having: Irregular respirations (caused by impaired brainstem function) Bradycardia. Hypertension (Widening Pulse Pressure)Subarachnoid hemorrhage as shown on a CT scan. It is denoted by the arrow. This type of injury may result in damage to the brainstem
32Subarachnoid hemorrhage Ninety percent of primary subarachnoid hemorrhages arise from congenitally derived arterial outpouchings (berry aneurysms) that lie at bifurcations of the major components of the circle of Willis. The most common sites are the carotid-posterior communicating and the anterior cerebral-anterior communicating artery junctions
34Clinical manifestations- differ or are similar for each syndrome Clinical manifestations- differ or are similar for each syndrome. Some are listed below:Contralateral Hemiparesis/hemiplegiaHomonymous HemanopiaReceptive/expressive aphasiaDrowsiness, stuporAgnosiaNeglect, inattention of double simultaneous stimulationSensory deficitsImpaired gaitFlat affect, disinhibition, personality change, loss of decision makingUrinary incontinenceSpeech preseverationDizzinessNystagmus & diplopiaDysphagia & dysarthriaPainIpsilateral numbness & weaknessClumsinessStaggering gait & ataxiaSyncopeApraxiaParalysis of the contralteral face, arm & leg
35Lacunar Strokes Include, but not limited to: Contralateral paresis or plegia of face, arm, or legContralateral decreased sensation of face, arm, or legSlurred speech, and weakness and ataxia of the armNumbnessCalled lacunar strokes because of the cavity that is created once the infarcted brain tissue disintegrates.
36Locked-In SyndromeBrainstem infarct or Pontine haemorrhage leaving the patient paralysed but with intact cortical function.Breathes spontaneously.Paralysis of horizontal eye movements but retains the ability to look up.Retained sensation in the limbs and hearingCheck for this by attempting to establish communication with the patient using upward eye movements. For example: “Look up once for Yes, look up twice for No”. Then, “Can you hear me?”
37SeizuresSeizures are an abnormal, sudden, excessive discharge of electrical activity within the brain.
38Dysphasia Diet Four (4) types of dysphagia diets. Link:Four (4) types of dysphagia diets.NDD Level 1: Dysphagia-Pureed (homogenous, very cohesive, pudding-like, requiring very little chewing ability).NDD Level 2: Dysphagia-Mechanical Altered (cohesive, moist, semisolid foods, requiring some chewing).NDD Level 3: Dysphagia-Advanced (soft foods that require more chewing ability). Regular (all foods allowed).National Dysphagia Diet – NDD – (What to swallow)
39Aspiration PneumoniaGeneral Guidelines for Aspiration Pneumonia preventionPatient should sit upright (45 degrees) for eatingEach bolus should be less than one teaspoonPlace food well into mouthEncourage patient to gently cough after each swallowPatient should swallow several times after each bolus
40Bladder & bowel Deficits Frequency, urgency and incontinencePotential for bladder retraining if cognitively intactAvoid catheterizationBowel – constipation (related more to immobility)
41Communication Deficits Motor Aphasia – Broca’s area- speak very little or not at all, no activation of muscles to produce speech, but can comprehend spoken or written language.Expressive aphasia: aka: non- fluent aphasia; unable to form words that are understandable; may be able to speak in single-word responses (Broca’s, frontal lobe)Sensory Aphasia- Wernicke's area- can speak but cannot understand spoken or written language. Speech is effortless but is garbled and incomprehensible.Receptive aphasia: aka: fluent aphasia; unable to comprehend the spoken word; can speak but may not make sense (Wernicke's, parietal lobe)Global (mixed) aphasia: Combination of both receptive and expressive aphasiaCommunication Deficits
42Management of TIA & CVA NON-SURGICAL & SURGICAL Timing is paramount when dealing with brain conditions
44Interventions: Neuroprotectants Control of fever Glycaemic control DVT preventionAspiration precautionsAvoidance of IDC’sBowel (&bladder) regimenEarly mobilisation
45Other Interventions Prevent joint deformities Establish an exercise programPrevent painEnhance self-careManage sensory-perceptual difficultiesManage dysphagiaImprove thought processesImprove communicationMaintain skin integrityImprove family copingAssist patient & partner with sexual dysfunction
46Nursing AssessmentNeurologically the patient will primarily be assessed thoroughly covering all anatomical systems, including neurologically ( e.g. Seidel’s Neuro assessment) PMH, 5 dimensions of health, medications and ADLS, IADL’s using a functional assessment (e.g. Barthels assessment).
49Cranial Nerve (CN)ProcedureCN I (olfactory)Test ability to identify familiar aromatic odors, one naris at a time with eyes closed.CN II (optic)Test vision with Snellen chart and Rosenbaum near vision chart.Perform ophthalmoscopic examination of fundi.CN III (oculomotor)Test visual fields by confrontation and extinction of vision.IV (trochlear) ***Inspect eyelids for drooping.***VI (abducens)***Inspect pupils' size for equality and their direct and consensual response to light and accommodation.***Test extraocular eye movements.CN V (trigeminal)***Inspect face for muscle atrophy and tremors.***Palpate jaw muscles for tone and strength when patient clenches teeth.*Test superficial pain and touch sensation in each branch*** (test temperature sensation if there are unexpected findings to pain or touch).Test corneal reflex.CN VII (facial)***Inspect symmetry of facial features with various expressions (e.g., smile, frown, puffed cheeks, wrinkled forehead).***Test ability to identify sweet and salty tastes on each side of tongue.CN VIII (acoustic)Test sense of hearing with whisper screening tests or by audiometry.Compare bone and air conduction of sound.Test for lateralization of sound.CN IX (glossopharyngeal)***Test ability to identify sour and bitter tastes.Test gag reflex and ability to swallow.***CN X (vagus)***Inspect palate and uvula for symmetry with speech sounds and gag reflex.***Observe for swallowing difficulty.***Evaluate quality of guttural speech sounds (presence of nasal or hoarse quality to voice).CN XI (spinal accessory)***Test trapezius muscle strength (shrug shoulders against resistance).***Test sternocleidomastoid muscle strength (turn head to each side against resistance).***CN XII (hypoglossal)***Inspect tongue in mouth and while protruded for symmetry, tremors, and atrophy.***Inspect tongue movement toward nose and chin.***Test tongue strength with index finger when tongue is pressed against cheek.***Evaluate quality of lingual speech sounds (l, t, d, n).
50Neurological Assessment Test Selective Cranial Nerves (See previous slide and highlighted areas)Cerebellar Function and Proprioception1. Evaluate coordination and fine motor skills by the followingRapid rhythmic alternating movementsAccuracy of upper and lower extremity movements2. Evaluate balance using the Romberg test & Heel-To-Toe test 3. Observe the patient's gaitPostureRhythm and sequence of stride and arm movementsSensory Function1. Test primary sensory responses to the following • Superficial touch • Superficial painSeidel (2006)
51Neurological Assessment conti’d 2. Evaluate perception of position sense with movement of the great toes or a finger on each hand 3. Assess ability to identify familiar object by touch and manipulation (stereognosis) 4. Assess two-point discrimination -not taught 5. Assess ability to identify letter or number “drawn” on palm of hand (graphesthesia) 6. Assess ability to identify body area when touched Superficial and Deep Tendon Reflexes - not taught 1. Test abdominal reflexes 2. Test the cremasteric reflex in male patients 3. Test the plantar reflex 4. Test the following deep tendon reflexes • Biceps • • Triceps • Patellar • Achilles 5. Test for ankle clonus
524+ Very brisk; hyperactive with clonus, indicative of disease Reflexes:4+ Very brisk; hyperactive with clonus, indicative of disease3+ Brisker than avg, may indicate disease2+ Average, normal1+ Diminished, low normal0 No responseClonus = set of short jerking contractions of the same muscle.