Stroke: Medical and Nursing Considerations Collins Uzuegbu, BSN, RN Wright State University, Winter, 2012 Objectives Gross anatomy of the head Detailed anatomy of the human brain and its circulation A look at assessment features and important diagnostic tests for stroke. Examine ischemic and hemorrhagic strokes and treatment. Present evidence from current practices.
A first look at the brains protective structures . The Human Skull Layers of the meninges There are 3 important spaces between these layers: Epidural space: btw the skull and dura mater Subdural space: btw the dura mater and arachnoid mater subarachnoid space: btw arachnoid space and pia mater. This is where the CSF flows Structures of the brain Cerebrum: made up of lobes and each lobe has
specific functions Structures of the brain Cerebrum Frontal lobe: eye movement, personality, judgment, speech. Brocas: formulation of words. Damage to this causes expressive aphasia. Parietal lobe: sensory awareness, touch, pain sensory processing. Temporal lobe: Hearing. Damage to the Wernickes area causes receptive aphasia.
Occipital lobe: vision. Detailed anatomy Basal ganglia: fine body movements Corpus callosum: connects both the right and left hemispheres. Diencephalon: located inside the cerebrum and houses the hypothalamus and thalamus. Thalamus: is at the top of the reticular activating system (RAS) and plays a vital role in sensing pain stimulus Detailed anatomy Hypothalamus: homeostasis regulation by interacting with
the pituitary gland. Regulates sex drive, temperature, heart rate, sleep cycle, blood pressure, and fluid balance. Cerebellum: located below the cerebrum, in the posterior fossa, connected by the cerebellar peduncles to the midbrain, pons, and medulla. For muscle control, and balance. Midbrain channels: directs the RAS to the thalamus. It is the origin of CN III & IV and modulates auditory and visual reflexes. Pons channels: channels the RAS to the midbrain. Modulates info on respiratory functions. It is the origin of CN V, VI, VII, & VIII. RAS: begins in the medulla which is the origin of CN IX, X, XI, & XII. The medulla regulates BP and respiration.
Review of anatomy 1. Cobweb structure that houses arteries and veins: A. Dura mater B. Arachnoid matter C. Pia mater Review of anatomy 2. Tough white layer that lines the interior of the skull. A. Dura mater B. Arachnoid mater C. Pia mater
Review of anatomy 3. Located below the cerebrum, in the posterior fossa that functions for muscle control, fine movements and balance. A. B. C. D. Diencephalon Corpus callosum Cerebellum
Thalamus Review of anatomy 4. Damage or injury to the frontal lobe would cause A. B. C. D. Speech and memory loss vision changes Change in personality Touch and pain awareness
Circulation in the brain CSF The CSF cushions the brain and spinal cord. Produced primarily in the choroid plexus (an area in the ventricles of the brain). Approximately 500 ml are made daily. Normal CSF pressure 75 180 mmHg. CSF is absorbed into the arachnoid villi Cerebral arteries
Cerebral arteries The posterior cerebral artery (PCA) supplies the occipital lobe, midbrain, thalamus, and the inferior medial temporal lobe. The middle cerebral artery (MCA) supplies the lateral areas of the frontal, temporal, and parietal lobes. The anterior cerebral artery (ACA) supplies the medial areas of the frontal, parietal and temporal lobes. Venous blood flows through the cerebral veins and the sinuses of the dura. Circulating volume
The brain circulates 750 ml of blood/ min per minute. The brain is incapable of storing oxygen and glucose Any disruption in blood flow may result in significant ischemia. Cerebral ischemia Global: loss of perfusion to a large area(s) of the brain Focal: loss of perfusion to small, localized area(s). Quick Circulation Review: ACA = medial areas of the frontal, parietal and temporal lobes
MCA = lateral areas of the frontal, parietal, and temporal lobes. PCA = occipital lobe, midbrain, thalamus, and the inferior medial temporal lobes. Monro-Kellie Hypothesis Monro-Kellies doctrine states that the sum of the volumes of the brain, CSF, and intracranial blood is constant. Any increase in one causes a decrease in one or both of the remaining two. (Bahram , 2001)
CPP and ICP CPP (cerebral perfusion pressure): CPP = MAP ICP. (Normal: 60-90). ICP (Intracranial pressure): Normal ICP range: 0-15 mmHg. ICP of > 40 mmHg is a medical emergency. Increased ICP/cushings triad: widening pulse pressure (hypertension), respiratory irregularity (cheyne stokes) and bradycardia. What happens when the brain/skull is full: high pressure?
1.Shunting CSF into the subarachnoid space, 2. Increased CSF absorption in the venous sinus through the arachnoid villi 3. Decreased CSF production in the choroid plexus. 4. Auto regulation Questions STROKE A serious reduction in brain perfusion caused by obstruction, stenosis, or
rupture of one or more vessels that supplies blood to the brain. It is sometimes referred to as brain attack. Epidemiology Stroke affects 700,000 people each year, killing over 160,000. It is the third leading cause of death and a major cause of disability in the U.S. It costs an estimated $43 billion yearly to treat stroke.
Modifiable and nonmodifiable risks Classification of Ischemic strokes Large artery artherosclerosis Cardioembolism Lacunar strokes (small vessel occlusion) Strokes of other determined etiology (cardiac arrest or pulmonary embolism) Stroke of undetermined etiology
Etiology, risk factors and patient management Large artery artherosclerosis Pathophysiology of artherosclerotic plaque formation Cardioembolism Blood clots from the heart causing brain infarction. Predisposing factors: valvular heart disease, atrial fibrillation, tumors, acute MI, and endocarditis.
Lacunar strokes Occlusion of one or more of these tiny (as shown) arteries results to the death of cells distal to them Intracerebral bleed This occurs with rupture of one of the blood vessels resulting to increased ICP and ischemia/infarction in brain parenchymal cells distal to the injured area. Subarachnoid hemorrhage (SAH)
Blood vessel ruptures in membranes surrounding the brain. Occurs in middle age. Would likely present with the most explosive headache imaginable. Signs of meningeal irritation seizures, photophobia, nuchal rigidity (meningeal irritation) or LOC may occur Checking Meningeal Irritation: Positive Kernigs sign
Positive Brudzinskis sign Review What is the most likely cause of Intracerebral bleed? A. AVM B. Cocaine use C. Fat embolism Aneurysm Results from a weak area in the artery that balloons. Common in areas of bifurcations such as the circle of willis.
The risk of rebleed is highest in the first 24 hours. Signs and symptoms of rebleed include, sudden onset of severe headache, n/v, decrease in LOC, and a new focal neurologic deficit. Prevention of vasospasm is very important Aneurysm treatment surgical clipping with titanium clips. Newer method is using Guglielmi Detachable Coil. (Pearl, Gregg, & Gailloud, 2010)
AVM Arteries and veins connect by nidus. AVMs may increase intercerebral pressure causing ischemia or they may leak or rupture causing ICH or SAH. Unruptured AVMs present as headaches/migraines, often unilateral. Sometimes this is the only presenting symptom. They are most likely to bleed btw later childhood and end of middle age, after which the risk for bleed starts decreasing. Once AVM has bled, the risk of rebleed in one year is 20% or less. This risk continues to decrease
overtime. No known causes but present from birth. Treatment of AVM Embolization: Retrograde thrombosis is a major risk). microsurgery: (only risk r/t anaesthesia) Stereotactic radiosurgery: there is risk of radiation toxicity. TIA caused by initial plaque fisure. With continued, persistent accumulation of clotts due to platelets aggregation and other
factors, ischemic stroke could develop. In ischemic brain tissue, membranes surrounding the ischemic tissue becomes leaky. loss of nutrients, anerobic respiration resumes It takes about 10 minutes for complete damage of the ischemic area to occur.. Question Which of the following describe AVM? a. an aneurysm occurring in the circle of willis b. a plaque fissure causing
temporary obstruction of blood flow c. masses of malformed blood vessels growing in the brain Zones of Injury Core ischemic zone: area directly injured ischemic penumbra: it is the area between healthy, perfusing cells and the injured or necrotic area. Presenting symptoms With stroke, SIZE and TIME matter.
1. Sudden weakness or numbness in one of both sides of the body 2. Sudden loss of speech or ability to comprehend 3. Changes in vision in one or both eyes 4. Unexplained dizziness or unsteadiness or falls 5. Sudden severe headache: worse headache of my life! Locations and deficits Middle artery occlusion: loss of movt or feeling in the contralateral side. Gaze preference in the ipsilateral side; lesion in the dominant side of the hemisphere causes receptive, expressive or global aphasia results. With
lesions on the non dominant hemisphere, neglect syndrome occurs. Partial occlusion results to partial deficits and partial aphasia. Posterior artery: two syndromes seen with midbrain, subthalamic and thalamic regions involved, the pt presents with third nerve palsy, weakness and palsy. If the infarct is extensive here, coma with decerebrate posturing may result. When the injury involves the medial temporal and occipital lobes, memory loss or vision in the contralateral sides occur. Basilar artery: TIA here may produce dizziness while total occlusion produces quardriplegia. Cerebellar artery: with superior cerebellar involvement, partial deafness, cerebellar ataxia, n/v, loss of pain and temperature sensation in the contralateral side (thalamus involved). Cranial nerves deficit may occur including dysphagia and loss of cough reflex.
Anterior artery: causes ipsilateral deafness, vertigo and facial weakness. Diagnosis Clinical pearl: 1. Any pt with sudden onset of neuro deficits should be evaluated for stroke. 2. There are no definite signs to differentiate ischemia, infarction, or hemorrhage. 3. Diagnose quickly and treat promptly. Hx:
Time of onset Recent events: stroke? Mi? recent surgeries/bleeds? comorbidities: DM?, HTN? Drug and alcohol use? meds review: anticoagulants? Insulin? Antihypertensives? Physical assessment:NIH Scale Physical assessment Continues Head/neck: meningeal irritation, trauma, recent infection? Heart: irregularities in beats,
carotid bruit? Neuro: LOC, mentation, cranial nerves, sensory and motor functions, cerebellar functions, deep tendon reflexes wnl for pt? Diagnostic studies non contrast brain ct or mri blood glucose CBC, BMP, RFP, Platelets (poss cause:leukemia, polycythemia, or stroke mimic low lytes etc?) EKG and Cardiac enzymes (Poss link btw high enzymes and ischemic stroke outcome)
PT/INR/APTT (coagulopathy hemorrhage? VS Diagnostic tests con.. CT For rtPA candidates, complete and interpret within 45 mins May see most hemorrhages or tumors may repeat if deficits continue Diffusion weighted MRI (DW MRI) Biggest benefit: lesions are seen within minutes of sx onset. These lesions are poorly seen on CT - AVMs are best seen with MRI - SAH diagnostics: lumbar puncture (LP) and CT. Do CT first in pts with suspected increased icp to reduce risk of
brain herniation. Most definitive dx is blood in CSF - May do carotid U/S for precerebral arteries suspected of occlusion or dissection Angiogram to investigate aneurysms Review Question: you suspect ischemic stroke, which diagnostic test will show you ischemic regions within minutes of sx onset? a. CT with contrast b. noncontrast CT C. DW MRI D. Cerebral angiogram
Nursing Consideration and pt management Goal of treatment is stabilize and minimize neuro deficits maintain adequate oxygenation Avoid hypercapnia cos leads to increased ICP. All pts with suspected stroke must get supplemental O2. Maintain O2 > 95% Keep HOB 30 degrees to avoid increase in ICP and minimize aspiration pt must cough and deep breathe to avoid atelectasis and PNA
When should you intubate? If GCS is 8 or less Evaluate for tissue plasminogen activator (TPA admin complete the checklist for TPA thoroughly and accurately. Ultimately the decision to administer rtpa or not is the clinicians call. Important patient management factors to consider related to rtpa administration Give only in a critical care setting Dose is 0.9 mg/kg with max of 90 mg. give 10% of the dose as a bolus over one minute then infuse the rest over 60 minutes. Must give within 3 hours of symptom onset. If after 3 hours, there is risk for hemorrhagic conversion of the stroke.
Neuro assessment every 15 mins during infusion, every 30 mins for the next 6 hours then hourly for the first 24 hrs. Monitor the BP alongside neuro checks. Check BP more frequently if > 180/105 mmHg. Give antihypertensive if necessary to keep BP at or below these values. If the pt develops severe headache, acute HTN, n/v, dc infusion and get STAT CT. Dont bother them with foleys or NGs for the moment. Get a follow up CT scan 24 hrs before starting antiplatelet or anticoags Special consideration in regard to BP management in a stroke pt - ischemic Treatment of BP within the first hrs of sx onset
Initiation of antihypertensive therapy is indicated in stroke pt who have MI, heart failure, renal failure, aortic dissection, hypertensive encephalopathy, and for pts receiving rtpa with BP > 180/105 mmHg. MAP in all cases should not be lowered more than 20 mmHg. BP mgt. If BP is > 180/105 mmHg in a candidate for rtpa, consider the following: Labetalol 10-20 mg ivp over 1-2 mins, repeat x1 if nec Nitro paste 1-2 inches Nicadipine infusion 5 mg/hr, titrate by 2.5 mg/hr every 5-15 mins; max dose 15 mg/hr. when desired
BP is achieved, reduce infusion bby 3 mg/hr. if bp does not come below 180/105, DO NOT GIVE rtpa. With high BP after rtpa therapy, 180-130/105-120, give Labetalol. If BP > 230/120, consider Labetalol or Sodium Nitroprusside. Hypotension Hypotension is rare in stroke pts and is assoc. with poor outcomes. It gets dangerous when its < 110/70 mmHg. May be corrected with cautionary fluid replacement.
Special consideration in regard to BP management in a stroke pt - hemorrhagic Keep BP btw 150-160 mmHg systolic. If BP is too low, vasospasm may occur. BP drugs are same as for ischemic stroke . Acute Management of vasospasm Correct hypervolemia (major cause of vasospasm) with crystalloids. Keep SBP >150 but not more than 185 (some institutions 180). Hemodilute Hct 30-35%.
Temperature management Hypothermia is neuroprotective May use antipyretics and or cooling blanket to lower temperature. If temp reaches 30-32, may result to hypotension, and cardiac dysrhythmias. Glycemic control Try to maintain blood glucose within normal (70-110) Below 50 may result to neuro deficits that may be confused for stroke. Hyperglycemia is associated with tissue acidosis and free radical production.
More things to consider Thrombectomy Control of ICP Relieve hydrocephalus Rehab: multi-disciplinary effort 1. Rehab starts in the critical care treatment area 2. Teach pt and family about: the pathophys of stroke; specific etiology; risk factor modification; 3. importance of taking meds; ADL performance; injury prevention for affected
limbs; how to compensate for residual deficits; basic rehab techniques and the importance to practice these techniques; and 4. encourage support group participation. Newer Rehab Efforts:EBP Gait Retraining Using a Treadmill Electrical Stimulation for the Hemiparetic Arm: Significantly improves passive and active ROM improves manual dexterity, motor function, and sensation improves shoulder strength significantly
improves use with ADL, including dressing, reaching, feeding, and tying knots (Richman, 2012; Richman, & Caple, 2012). Drug Pharm Review Recombinant Tissue plasminogen activator (rtpa) EG. Tenecteplase and alteplase
Class Dosage Thrombolytic TNKase 50mg Powder for Injection *0.9 mg/kg total with with 10 % given IV over 1 min and 90% given by continuous infusion over 1 hr Pharmacology
Special Consideration Exerts thrombolytic action on the endogenous fibrinolytic system to convert plasminogen to plasmin, which in turn degrades the fibrin strands, essentially, crashing party for the coagulation cascade.
Unlike streptokinase or urokinase, most of the activity of alteplase or tenecteplase is dependent on the presence of fibrin. Eliminated by hepatic metabolism. The initial half-life is about 2024 minutes, followed by a terminal half-life 1.Start 3 hrs of sx
onset 2.Dont give more than 90 mg 3. dont use any other anticoags for 24 hrs 4. monitor pt closely What rtpa does: crashes party for the coagulation cascade (Satyan, 1999) Drug
.. Labetalol Class Dosage Pharmacology Special Consideration Its a competitive,
nonselective betaadrenergic and selective postsynaptic alpha-1adrenergic receptor blocker Comes in 100-300 mg tabs, and 5mg/ ml IV Administer labetalol slowly by IV infusion, initially at
2 mg/minute, then adjust for pts supine BP. For IVP, give slowly over 510 mins. IV max: 300 mg dose. Sympatholytic, antianginal, and antihypertensive. Labetalol acts on alpha- and betareceptors leading to vasodilation and decreased total peripheral resistance,
which results in decreased blood pressure without a substantial decrease in resting heart rate, cardiac output, or stroke volume. Its extensively metabolized in the liver. half-life in patients with normal renal function ranges from 2.58 hours
1.Pt must be supine during iv admin 2. Watch for dyspnea and wheezing prob due to Labetalol effect on bronchial smooth muscle. 3. may result to importence 4. watch for hypotension and brady
Drug Class Dosage Pharmacology Special Consideration Nitro paste Organic nitrate: gold standard in
the management of angina pectoris Comes as Nitroglycerin topical 2%. Administer 1-2 inches. Nitroglycerine induces dephosphorylation (removes phosphate from CGMP) of the
myosin light chain and causes the cell to release calcium, thereby relaxing the smooth muscle cells and producing vasodilation. Duration of action 4-8 hrs (for ointment) and 18-24 hrs for paste. **Side note: may be used to treat pain r/t hemorrhoids and
relaxant aid for retained placenta? 1.monitor for headaches r/t vasodilation 2. Remove patch prior to defib or mri. Some patches contain aluminium and may burn pt or damage paddle. 3. Do not massage after application. May cause too quick an
effect. 4. Do not touch with bare hands Drug Class Dosage Pharmacology Special Consideration
Sodium Nitroprusside Powerful vasodilator Comes in 50 mg/2ml injection. Start at 0.5 mcg/kg/ min as an IV infusion, and increase by 0.5 1.5 mcg/kg/min at 5 minute intervals
(max: 10 mcg/kg/min for 10 minutes) Acts directly on peripheral arterial and venous smooth muscles, causing significant vasodilation. It also causes slight decrease in HR and CO (due to venous pooling and
decreased arterial resistance). it does not affect myocardial contractility. Used to manage hypertensive emergencies. Reduces preload and afterload. Metabolized by the liver. 1.Infusion must be brief. Prolonged infusion leads to massive toxicity
including coma, mydriasis, absent reflexes, n/v, dysphagia (due to overwhelming production of its metabolites cyanide and thiocyanate). 2.must watch for hypotension. 3. Do not infuse alongside Epi; may counteract hypotensive action
(Epi is the only med that can counter Na+ Nitroprusside). 3. monitor Na+ levels due to increased diuresis with Na+ Nitroprusside. 4. You can almost always maintain any BP level with various infusion rates of this medication References
American Association of Critical Care Nurses, A. (2011).Essentials of critical care orientation. Retrieved from http://www.healthstream.com/HLCSCP/hstmfiles/hstmdeliver.aspx?configuration=1|702b96a7- 71bd-db11- bf7b000423d6b5c1|Falseistration=ea0b87d1-ed5d-e111-9404-0015171c5bb1 Bahram , M. (2001). The monrokellie hypothesis: Applications in csf volume depletion. Neurology , 56, 1746-1748. Retrieved from http://www.neurology.org/content/56/12/1746.full.pdf html
Elsevier /Goldstandard. (2012). Clinical PharmacologyRetrieved from http:// www.clinicalpharmacologyip.com/default.aspx. Gustavo, et. al, (2011). Diagnosis and management of cerebral venous thrombosis: A statement for healthcare professionals from the american heart association/american stroke association. Stroke, 2011(42), 11581192. doi: doi: 10.1161/STR.0b013e31820a8364
McCance, K. L., & Huether, S. E. (2006). Pathophysiology, the biologic basis for disease in adults and children. (Fifth ed.). St. Louis, Missouri: Mosby Inc. References Mokri, B. (2001). The Monro-Kellie hypothesis: applications in CSF volume depletion. Neurology, 56(12), 1746-1748. Pearl, M., Gregg, L., & Gailloud, P. (2010). Endovascular treatment of aneurysmal subarachnoid hemorrhage. Neurosurgery Clinics Of North America, 21(2), 271-280. doi:10.1016/j.nec.2009.10.004
Richman, S., & Caple, C. (2012). Stroke Rehabilitation: Gait Retraining Using a Treadmill. Richman, S. (2012). Stroke Rehabilitation: Electrical Stimulation for the Hemiparetic Arm. Urden, L., Stacy, K. M., & Lough, M. E. (2006). Thelan's critical care nursing: Diagnosis and management. (5 ed.). St. Louis, MO: Mosby Elsevier.
Satyan, M. (1999). The coagulation cascade: Physiology, disorders, evaluation.. Unpublished manuscript, Department of internal medicine, University of Florida, Retrieved from http://medinfo.ufl.edu/year2/coag/title.html
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