Presentation on theme: "Ida Shepherd. Define various neurological conditions Identify risk factors for stroke Describe the functions of each of the 4 brain lobes List the mechanisms."— Presentation transcript:
Define various neurological conditions Identify risk factors for stroke Describe the functions of each of the 4 brain lobes List the mechanisms of ischaemic cell injury Differentiate between subarachnoid and intracerebral haemorrhagic strokes Describe the pathology of TIA’s Compare & contrast 5 types of CVA Identify the physiological/cognitive effects of a CVA Describe the nursing interventions for patients experiencing a CVA or post-CVA Describe 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 assessment
Cerebrovascular 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.
Reversible 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 days Completed Stroke-Patient appears stable with neurologic deficit permanent and unchanging
Cerebrovascular 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. http://www.health.govt.nz/publication/mortality-and-demographic-data-2006 http://www.health.govt.nz/publication/mortality-and-demographic-data-2006
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.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.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.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.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/stroke-facts-and-fallacies
Stroke 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 http://www.stroke.org.nz/resources/NZClinicalGuidelinesStrokeManagement2010ActiveContents.pdf http://www.stroke.org.nz/resources/NZClinicalGuidelinesStrokeManagement2010ActiveContents.pdf
Significant 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).
Pacific 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). http://www.stroke.org.nz/resources/NZClinicalGuidelinesStrokeManagement2010ActiveContents.pdf http://www.stroke.org.nz/resources/NZClinicalGuidelinesStrokeManagement2010ActiveContents.pdf
Age Male Race Heart Disease & AF Diabetes ↑ hematocrit or other hypercoagulability states Earlier stroke or TIA Asymptomatic carotid artery stenosis Hypertension Oral contraceptive use (especially if a smoker) Family history Excessive ETOH intake Drug abuse Obesity Sedentary lifestyle Elevated serum cholesterol & triglycerides Migraines Cigarette smoking Sickle cell disease
Carotids supply anterior portion of brain. Vertebral - basilar artery and supplies the posterior portions of the brain.
Optimal Cerebral Perfusion Pressure (CPP) has a MAP of 50mmHg which is maintained with 750-1000mL 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 & CO 2 retention. A complex cascade of biochemical changes occur in response to the ischemia
1. Interruption of oxygenated blood flow to an area of the tissue (heart, brain, limb) (cerebral blood flow falls to less than 25mL/100g/min) 2. Oxygen tension within cell decreases leading to decreased ATP 3. Local acidosis build-up, pH levels change 4. Failure of sodium pump, decreased potassium 5. Influx of sodium and water into cell causing swelling 6. Progressive loss of glycogen and protein synthesis 7. Morphologic deterioration (cell structure begins to degenerate) 8. Mitochondria begin to swell, EPR dilates 9. Glutamate released causing further cell damage Reversible to this point with reperfusion of tissues
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, syncope Post 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 Scorecard
Ischemic 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.
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
Subarachnoid haemorrhagic stroke - bleeding into subarachnoid space. - usually rupture of cerebral aneurysm or arteriovenous malformation Intracerebral 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)
10 percent of stroke survivors recover almost completely 25 percent recover with minor impairments 40 percent experience moderate to severe impairments requiring special care 10 percent require care in a nursing home or other long-term care facility 15 percent die shortly after the stroke
Early indicators of IICPLate indicators of IICP Alteration in LOC ranging from irritability, restlessness, and confusion to lethargy Possible onset or worsening of headache Beginning pupillary dysfunction, such as sluggishness; visual disturbances, such as diplopia or blurred vision Onset 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 vomiting Hemiplegia; posturing Alterations 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; papilledema Impaired brainstem reflexes (corneal, gag, swallowing).
Increased 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.
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.
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 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
Include, but not limited to: Contralateral paresis or plegia of face, arm, or leg Contralateral decreased sensation of face, arm, or leg Slurred speech, and weakness and ataxia of the arm Numbness
Brainstem 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 hearing Check 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?”
Link: http://www.asha.org/Publications/leader/2003/031104/f031104c.htm http://www.asha.org/Publications/leader/2003/031104/f031104c.htm 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).
General Guidelines for Aspiration Pneumonia preventionAspiration Pneumonia Patient should sit upright (45 degrees) for eating Each bolus should be less than one teaspoon Place food well into mouth Encourage patient to gently cough after each swallow Patient should swallow several times after each bolus
Frequency, urgency and incontinence Potential for bladder retraining if cognitively intact Avoid catheterization Bowel – constipation (related more to immobility)
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 aphasia
NON-SURGICAL & SURGICAL Timing is paramount when dealing with brain conditions
1. Neuroprotectants 2. Control of fever 3. Glycaemic control 4. DVT prevention 5. Aspiration precautions 6. Avoidance of IDC’s 7. Bowel (&bladder) regimen 8. Early mobilisation
9. Prevent joint deformities 10. Establish an exercise program 11. Prevent pain 12. Enhance self-care 13. Manage sensory-perceptual difficulties 14. Manage dysphagia 15. Improve thought processes 16. Improve communication 17. Maintain skin integrity 18. Improve family coping 19. Assist patient & partner with sexual dysfunction
Neurologically 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).
Cranial Nerve (CN)Procedure CN 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).
Test Selective Cranial Nerves (See previous slide and highlighted areas) Cerebellar Function and Proprioception 1.Evaluate coordination and fine motor skills by the following Rapid rhythmic alternating movements Accuracy of upper and lower extremity movements 2.Evaluate balance using the Romberg test & Heel-To-Toe test 3.Observe the patient's gait Posture Rhythm and sequence of stride and arm movements Sensory Function 1.Test primary sensory responses to the following Superficial touch Superficial pain Seidel (2006) http://www.nursingconsult.com/das/book/0/view/1373/325.html/top
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
Reflexes: 4+ Very brisk; hyperactive with clonus, indicative of disease 3+ Brisker than avg, may indicate disease 2+ Average, normal 1+ Diminished, low normal 0 No response