MVC-AACN Newsletter
FALL 2013
Inside This Issue1-2 / Letter from New Chapter President
2 / NTI News
3-11 / Neuro Program Review
11 / Horizons Reminder
12 / Step Forward Theme & Fall Program Reminder
13 / Fall Education program reminder
13-14 / Photos
Newsletter 4
Mary Kay next presented a brief presentation on coma, differentiating between deep coma, where the patient does not respond to pain or light coma where there is a response to noxious stimuli. There are multiple etiologies but she asked us to keep in mind that unilateral hemispheric lesions do not result in coma. The main interventions are to secure airway, establish IV access, consider dextrose or narcan, and MONITOR THE PATIENT.
Care of the ischemic stroke victim was the next topic reviewed. Stroke is defined as an abrupt and dramatic development of a focal neurological deficit caused by either an occlusion of an artery or rupture of the artery with blood escaping into the brain and/or subarachnoid space. Stroke is the 4th leading cause of death in the U.S. 20% of survivors still require institutional care after 3 months and 25 – 30% are permanently disabled.
The Stroke Chain of Survival encompasses 4 steps that involve the participation and cooperation of EMS providers:
1. Detection : understand the stroke signs/symptoms and determine TIME LAST SEEN NORMAL
2. Dispatch: public needs to understand the importance of 911
3. Delivery: initial patient stabilization and exclusion of other alternative etiologies
4. Door: patients should be delivered to a hospital competent to deal with stroke
There are non-modifiable risk factors for ischemic vascular events, such as age, sex, race, ethnicity, and family history of stroke/TIA. Many risk factors are modifiable however and the public needs to be educated about factors such as HTN, cigarette smoking, diabetes, dyslipidemia, atrial fibrillation, and cardiovascular disease. We, as nurses can educate our patients and the public so they can better understand the consequences of these factors and adhere to their treatment programs.
Patients may experience a TIA, defined by the AHA as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarct. Symptoms generally resolve in less than 24 hours and there is no radiographic evidence of insult on CT scan. These episodes need to be taken seriously however as 10 – 15% of TIA patients will have a stroke within 3 months (1/2 within 48 hours).
Ischemic stroke may be thrombotic, related to atherosclerosis or embolic in origin, related to DVT or atrial fibrillation. Thrombotic events are associated with sleep, while embolic are more associated with activity. Lacunar or subcortical strokes (small vessel disease) are very common in diabetic patients. The classic signs and symptoms of stroke are weakness of an arm/leg, difficulty speaking, headache, droopy smile, visual problems, and or numbness/tingling on one side of body.
The specific blood vessel affected in the brain and whether this is located in the dominant or non-dominant hemisphere determines the symptoms. Once a vessel is occluded, systemic arterial blood pressure influences cerebral perfusion pressure (CPP) and collateral blood flow during ischemia. Permanent ischemic cell death ensues after thirty minutes – continued ischemia (<50% of baseline CBF) will kill the rest of the vessel territory. Edema and increased ICP occurs as the natural evolution of insult and will be minimized if perfusion is restored.
There are 3 pathophysiological issues related to stroke – blood pressure (B/P), blood glucose, and temperature. Brain perfusion is dependent on mean arterial pressure (MAP). Increase in B/P may be the normal homeostatic response to stroke and usually falls spontaneously within 24 hours to several days. If the patient has not received thrombolytics, do not treat B/P in acute ischemic stroke unless systolic 220 mm Hg, diastolic B/P >120 mm Hg, or MAP >130 mm Hg. If thrombolytic therapy is to be used, do not treat unless systolic B/P >185 mm Hg (after TPA, 180 mm Hg), diastolic B/P >110 mm Hg (after TPA, 105 MM Hg).
Regarding blood glucose and stroke, when level exceeds 180, begin strategies to lower serum glucose. The New England Journal of Medicine published the results of a clinical trial stating a blood glucose target of 180 mg or < /deciliter resulted in lower mortality than did a range of 81-108 mg/deciliter. Hyperthermia has been found to increase mortality and length of stay (LOS) in the stroke patient. Temperature should be maintained 98.6 or <, IV Acetaminophen 1 gm q6 hours may be used to achieve this goal.
Hospitals must have an organized Stroke Intervention Program in place to ensure rapid identification and work up once the patient presents with possible stroke. Time of symptom onset is crucial and will direct course of treatment. Once the Stroke Team is activated and patient arrives in the ED, primary/secondary survey is completed. A complete NIHSS must be done by ED MD or primary nurse. Mini NIHSS and vital signs should be done q 15 minutes x1 hour. Notification of Neurologist should be done within 15 minutes of arrival in ED.
Immediate diagnostic studies for the patient with suspected stroke include non-contrast CT Scan (CT scan within 25 minutes of patient arrival with interpretation within 45 minutes of arrival) or MRI of the brain, Blood glucose, O2 saturation, serum electrolytes/renal function tests, CBC, platelets, PT/INR, PTT, EKG, and cardiac markers if necessary. There are conditions that mimic stroke which need to be ruled out, such as ICH, Todd’s paralysis (post seizure), hypoglycemia, complicated migraine, brain tumor, brain abscess, encephalitis, conversion disorder, or malingering.
Intravenous TPA is indicated for the treatment of acute ischemic stroke if patient symptoms began <4.5 hours prior to arrival, CT scan excludes hemorrhage, NIHSS 4 OR <, AGE >18, or isolated aphasia present. The exclusions for use of 3 – 4.5 hour IV TPA are age 80, patient taking oral anticoagulants, NIHSS > 25, or combination of prior stroke and diabetes. If the treatment decision is IV TPA, a second IV line should be initiated for thrombolytic, NIHSS q15 minutes needs to be continued, obtain/estimate weight, and avoid invasive tubes. IV TPA 0.9 mg/kg is given, 10% as IV bolus over 1-2 minutes followed by 90% over 60 minutes.
Post IV TPA care continues in the ICU. Neurological checks and vital signs are checked q15 minutes x 2 hours, q 30 minutes x 6 hours, then q 1 hour. Labetalol or Nicardipine are the drugs of choice to control B/P if needed. Nipride should not be used as it increases ICP. No invasive tubes should be inserted x 24 hours. Antithrombotic/antiplatelet drugs should not be given (ASA, Heparin, Warfarin, Ticlid, Lovenox, Plavix, Aggrenox, Fragmin are examples). Antiplatelet therapy may be started 24 hours after TPA. Also keep the patient NPO until a swallow evaluation is done, monitor blood glucose levels q 4 hours x2, maintain normothermia, and initiate TED hose/ compression boots for DVT prophylaxis.
Intra-arterial thrombolytic therapy to the occluded cerebral vessel may be a treatment option if the time window is < 6 hours from onset of symptoms. This requires availability of cerebral angiogram and a trained Interventional Radiologist. Removal of the intra- cerebral vessel clot may be done utilizing the Merci device especially if TPA cannot be given secondary to contraindications. This would generally be done in a tertiary health center.
If the acute ischemic stroke patient presents to the ED > 6 hours after symptom onset, primary/secondary assessment is performed and ASA 325 mg PR may be administered after hemorrhage is ruled out by CT scan. B/P management is done as previously discussed and the patient is kept NPO until dysphagia screen performed. Admission to a telemetry/ stroke unit for the first 24 hours is appropriate.
Hemorrhagic stroke accounts for 10 -20% of all strokes and has a 30 day morbidity rate of 43%. Hemorrhagic stroke may be intracerebral or subarachnoid (secondary to aneurysm or vascular malformations). Systemic HTN is the number 1 risk factor of intracranial hemorrhage (ICH) – other etiologies include brain tumors (commonly malignant), and cerebral amyloid angiopathy (pathological deposits of beta amyloid protein within the walls of small meningeal and cortical vessels – common in folks > 70, with anticoagulant use, vasculitis, venous infarction, and drug abuse such as cocaine or amphetamines). The hematoma releases toxins into brain tissue causing a local decrease in perfusion and cellular changes. Cerebral edema develops over 24 – 72 hours and ICP increases because of the space occupying blood clot. Intraventricular ICP monitoring/drainage may be utilized in the course of treatment.
The patient with an ICH may present with the sudden onset of focal deficit, severe headache, n/v, and/or decreased LOC.ICH in the cerebellum usually presents with severe headache, nuchal rigidity, n/v, balance/coordination problems and may progress to posturing and coma - this is best emergently treated in the OR. Coagulopathy may need to be reversed, and is managed depending on anticoagulant or antiplatelet agent used. If CT scan confirms hemorrhage, treatment will be determined by several factors such as patient age, pre-morbid condition, location and size of ICH, and patient’s advanced directive. If aggressive interventions are warranted, Mary Kay advised getting the Neurosurgeon involved.
If the patient has decreased LOC, unable to maintain a patent airway, motor score 5, or PaCo2 > 45, rapid sequence intubation (RSI) should be performed. Do not hyperventilate the patient - keep PaCo2 >35. B/P management may require placement of an arterial catheter for closer monitoring – systolic B/P should be kept < 150 mm Hg. IV Labetalol or Nicardipine are the agents of choice. Mannitol or 200 ml hypertonic saline (3%) over 20 minutes can be administered if patient exhibits signs of posturing, blown pupil, or increasing ICP by monitor.
When monitoring ICP, be aware of CPP (MAP –ICP) as this can reflect increased brain ischemia. Normal CPP range is 50 – 70. The patient needs to be kept euvolemic – do not dehydrate. Prophylactic anticonvulsant treatment is not recommended. Treatment with benzodiazepines is appropriate for actual seizures, also consider EEG monitoring if the patient’s LOC is worse than likely explained by the size and location of the hemorrhage.
Aneurysmal subarachnoid hemorrhage (SAH) occurs when a sacular outpouching of a cerebral artery ruptures into the subarachnoid space. The 30 day mortality rate with this bleed is 45%, with 30% of survivors left with a major disability. Associated risk factors are current smoking, HTN, women affected > men, African- American descent, family history, older age, excess alcohol intake/drug use. Higher risk of aneurysm formation and rupture are also associated with trauma to the vessel, polycystic kidney disease, connective tissue disease, and Ehler Danlos Syndrome, Type 4. The patient presents with the abrupt onset of “the worst headache of my life”, photophobia, stiff neck secondary to meningeal irritation, cranial nerve dysfunction, motor weakness to posturing, decreased LOC to coma (that can change in a second!).
Aneurysmal SAH is graded most commonly using the Hunt and Hess scale (1-4 depending on symptoms). Good outcomes are correlated with scores of 1 – 2 and worse outcomes with scores of 3 and 4. CT scan is the initial diagnostic study of choice. CT Angiogram affords rapid visualization of arterial anatomy, a 3 dimensional image that assists in determining the shape of the aneurysm prior to therapeutic intervention.
The greatest risk of re-bleeding occurs in the first 24 hours and at 7 – 10 days after initial SAH when clot lysis occurs. Early surgical or endovascular repair is the most effective intervention to prevent re-bleed. Surgical repair can be accomplished by clipping of the aneurysm neck or aneurysms not amenable to clipping may be resected or wrapped to reinforce the vessel wall. Interventional Neuro-radiologists may insert devices such as coils detachable balloons, and/or stents to occlude the aneurysm. A Ventriculostomy tube may be placed for high grade SAH, hydrocephalus, or increasing ICP enabling CSF drainage.
Cerebral vasospasm is a potential complication of aneurysmal rupture. Narrowing of cerebral arteries around the Circle of Willis causes an increase in velocities of arteries, decreasing blood delivery to cerebral tissue and may cause brain ischemia and infarct. Incidence and degree of vaso- spasm are directly related to amount of blood in the subarachnoid space. This can occur 4 - 14 days post rupture. Neurological symptoms may not occur or there may be subtle or dramatic deterioration in neurological function. Transcranial Doppler studies (TCD), usually done daily for 14 days after SAH may detect vasospasm. Cerebral angiography is used to diagnose or confirm vasospasm, or in the comatose patient brain tissue partial pressure of oxygen or CBF decrease if sensor is in the region fed by the spastic vessel. Nimodipine is given immediately after SAH diagnosis to reduce vasospasm and improve long term outcomes. Dosage is 60 mg q 4 hours or if hypotension, 30 mg q 2 hours x 21 days.” Double H” therapy is now used (hypertension and hemodilution), not “Triple H” (patient should be kept euvolemic). Statins may also be used to counter act vasospasm.
Another potential complication of aneurysmal SAH is myocardial stunning or Tako-tsubo cardiomyopathy and neurogenic pulmonary edema related to increased catecholamine release from a huge bleed. The treatment is supportive with goal of unloading the left ventricle – use contractility agents if possible such as dobutamine and a diuretic.