Cerebrovascular Accident I. I

Cerebrovascular Accident
I. INTRODUCTION
The world as a whole has been facing different constant changes not only in the environment but also in people’s lives. As changes occur, the more people become in need to adopt with these changes, thus, and we expose ourselves to illness that could even lead to unwanted events in our lives.
Our nursing case presentation is about Cerebrovascular Accident discussing Ischemic stroke. The content includes the patient’s general data and physical assessment, anatomy, physiology and pathophysiology, review of related literature, laboratory and pharmacology.
The highlight if the presentation deals with the nursing care presentation with the nursing care plan of our patient revolving on his priority nursing problems, goals of care, appropriate nursing intervention and its feedback evaluation.
Our group is composed of 11 Nursing students. We have chosen this case as a help for studies to eliminating and prevent through health education the enlarging occurrence of Cerebrovascular diseases like this.
We greatly acknowledge the cooperation extended by the patient. We also appreciate the effort of Our Lady of Fatima University Medical Center staff and the guidance provided to us by our Clinical Instructor, Mrs. Anna Liza Morales, and most importantly, we thank our God Almighty for all the graces he bestowed on us.

II. GENERAL DATA
Name: Estrellia, Remedios Salazar
Age: 54
Civil Status: F
Date of Birth: October 25 1956
Place of Birth: Valenzuela City
Nationality: Filipino
Religion: Roman Catholic
Address: 618 Caloong I, Valenzuela City
Date of Admission: December 6 2010
Date of Discharge: December 10 2010
Admitting Diagnosis: Cerebrovascular Accident
Physician-in-charge: Dra. Rebecca W. Deguyo, MD

Chief Complaint: HEADACHE

History of Present Illness:
One day prior to admission, patient complained of headache, associated with nape pain and dizziness. There was also a noted limitation of motion of the neck area. There was no associated vomiting, blurring of vision and loss of consciousness. No medications taken and no consult were done.
Few hours prior to admission, above symptoms have persisted which prompted patient to seek consult of his physician’s clinic. Patient was advised to be admitted for further evaluation and management, hence the subsequent admission.

Past Medical History:
(+) HPN- DX 2002
-on maintenance medication
(-) DM
(-) Asthma
(+) Previous hospitalization 2007 FUMC
(+) CVO Bleed -CVD bleed vs. infarct

Personal/ Social History:
(-) Smoker
(-) Alcoholic drinker

Family History:
(+) HPN on both sides
(+) DM on mother side
(+) CA both sides
-Cervical CA, Breast CA

III. PHYSICAL ASSESSMENT
Done on Admission: December 6 2010
General Assessment:
Conscious, coherent, ambulatory, NICRD.
General Survey:
Musculoskeletal disorder
R/to CVD re-intant
S/p CVD infarct
Left with sensory deficit
Right extremely.
Vital Signs:
BP: 100/90
PR: 81
RR: 18
Temp: 36.8
Skin:
Warm, with good skin turgor and skin texture, moist
HEENT:
PPC, AS.
(-) CLAD
(-) TPC
Neck:
(+) Limitation of the RAM of neck
Chest:
SCE,
(-) Retractor CBS
Heart
AP, NARR,
(-) murmurs
Abdomen:
Flabby, nabs, soft
(-) tenderness
Extremities:
GME
(-) edema
(-) cyanosis
PEP
Neurological Examinations:
Cerebrum: Convulsion, coherent for 3 spheres
Cerebellum: Can perform RAM
No nystagmus
Impression t/c CVD bleed vs. infarct.
Cranial Nerves:
I N/A
II PERTL 2-3 mm
III, IV, VI Intact EDMs
V Intact bicorneal reflexes
VII No facial symmetry
VIII Can hear
IX, X Can swallow
XI Can shrug shoulders
XII Tongue at the midline

Motor
R L
5/5 5/5
5/5 5/5
Sensory
R L
75 % 100 %

75 % 100 %

IV. ANATOMY AND PHYSIOLOGY

A. Anatomy of the Brain

Figure 4.1. The Anatomy of the Brain

The cranium
The brain is protected by a bony covering called the cranium (which, along with the bones of the face, makes up the skull). Inside the cranium, the brain is surrounded by the meninges. The meninges are made up of 3 layers of tissue:
* Pia mater – the layer closest to the surface of the brain
* Arachnoid membrane – the middle layer of tissue
* Dura mater – the outer-most layer
The cerebrum – the front of the brain
The largest part of the brain located in the front is called the cerebrum. The cerebrum is responsible for:
* Movement
* Body temperature
* Touch
* Vision
* Hearing
* Judgment
* Reasoning
* Problem solving
* Emotions
* Learning
The cerebrum has 2 parts: the right cerebral hemisphere and the left cerebral hemisphere. They are connected at the bottom and have a deep groove running between them. In general, the right cerebral hemisphere controls the left side of the body, and the left cerebral hemisphere controls the right. The right side is involved with creativity and artistic abilities. The left side is important for logic and rational thinking.
The hemispheres of the cerebrum are divided into lobes, or broad regions of the brain. Each lobe is responsible for a variety of bodily functions:
* Frontal lobes are involved with personality, speech, and motor development
* Temporal lobes are responsible for memory, language and speech functions
* Parietal lobes are involved with sensation
* Occipital lobes are the primary vision centers
The surface of the cerebrum appears wrinkled and is made up of deep grooves (called sulci) and bumps or folds (called gyri). The outer part of the cerebrum is called gray matter and contains nerve cells. The inner part is called white matter and contains connections of nerves.
The brainstem – the middle of the brain
The brainstem is located in front of the cerebellum. The brainstem is like the hard-drive of a computer. It is the main control panel for the body that passes messages back and forth between the brain and other parts of the body. The cerebrum, the cerebellum, and the spinal cord are all connected to the brainstem. The brainstem has three main parts, the midbrain, the pons, and the medulla oblongata.
The brainstem controls vital functions of the body, including:
* Breathing
* Consciousness
* Cardiac function
* Involuntary muscle movements
* Swallowing
* Movement of the eyes and mouth
* Relaying sensory messages (pain, heat, noise, etc.)
* Hunger
The cerebellum – the back of the brain
Behind the cerebrum at the back of the head is the cerebellum. In Latin, cerebellum means “little brain.” However, the cerebellum contains more nerve cells than both hemispheres combined. The cerebellum is primarily a movement control center, responsible for:
* Voluntary muscle movements
* Fine motor skills
* Maintaining balance, posture, and equilibrium
* Unlike the cerebrum, the left cerebellum controls the left side of the body, and the right cerebellum controls the right side of the body.
Unlike the cerebrum, the left cerebellum controls the left side of the body, and the right cerebellum controls the right side of the body.

Figure 4.2. The Motor, Sensory and Association Areas of the Cerebral Cortex.

Other important parts of the brain
Ventricular system. The brain is not a solid organ. There are fluid-filled cavities within the brain called ventricles. The ventricles are important in providing nourishment to the brain. The ventricular system produces and processes cerebrospinal fluid – a clear, watery substance that flows around the brain and helps cushion and protect it.
Cranial nerves. The brain also contains 12 pairs of cranial nerves each responsible for specific functions in the body:
* Olfactory nerve – smell
* Optic nerve – vision
* Oculomotor – eye movements, eyelid opening
* Trochlear – eye movements
* Trigeminal – facial sensations, chewing
* Abducens – eye movements
* Facial – taste, facial expressions
* Vestibulocochlear – hearing, balance
* Glossopharyngeal – taste, swallowing
* Vagus – swallowing, taste
* Accessory – neck and shoulder muscles
* Hypoglossal – tongue movement
Pituitary gland. The pituitary gland is located in the center of the brain and is about the size of a dime. The pituitary gland, often referred to as the “master gland,” is responsible for a number of functions including producing hormones for the thyroid and adrenal glands, as well as the hormones responsible for normal growth and sexual maturation.

B. Cerebral Circulation
The cerebral circulation receives approximately 15% of the cardiac output, or 750 ml per minute. The brain does not store nutrients and has a high metabolic demand that requires the high blood flow. The brain’s blood pathway is unique because it flows against gravity; its arteries fill from below and the veins drain from above. In contrast to other organs that may tolerate decrease in blood flow because of their adequate collateral circulation, the brain lacks additional collateral blood flow, which may result in irreversible tissue damage when blood flow is occluded for even short periods of time.
Arteries. Two internal carotid arteries and vertebral arteries and their extensive system of branches provide the blood supply to the brain. The internal carotids arise from the bifurcation of the common carotid and supply much of the anterior circulation of the brain. The vertebral arteries branch from the subclavian arteries, flow back to and upward on either side of the cervical vertebrae, enters the cranium through the foramen magnum. The vertebral arteries join to become the basilar artery at the level of the brain stem; the basilar artery divides to form the two branches of the posterior cerebral arteries. The vertebrobasilar arteries supply most of the posterior circulation of the brain.
At the base of the brain surrounding the pituitary gland, a ring of arteries is formed between the vertebral and internal carotid artery chains. This ring is called the circle of Willis and is formed from the branches of the internal carotid artery, and anterior and middle cerebral arteries, and anterior and anterior and posterior communicating arteries. Functionally, the posterior portion of the circulation and the anterior or carotid circulation usually remain separate. The arteries of the circle of Willis can provide collateral circulation if one or more of the four vessels supplying to become occluded or are ligated.
The arterial anastomoses along the circle of Willis are frequent sites of aneurysms. Theses can be formed when the pressure at a weakened arterial wall causes the artery to balloon out. Aneurysms may be congenital or the result of degenerative changes in the vessel wall associated with atherosclerotic vascular disease. If an artery with an aneurysm bursts or becomes occluded by vasospasm, an embolus, or a thrombus, the neurons distal to the occlusion are deprived f their blood supply and the cells die quickly. The result is hemorrhagic stroke (cerebrovascular accident or infarction). The effects of the occlusion depend on which vessels are involved and which areas of the brain these vessels supply.
Veins. Venous drainage for the brain does not follow the arterial circulation as in other body structures. The veins reach the brain’s surface, join larger veins, then cross the subarachnoid space and empty into the dural sinuses, which are vascular channels lying within the tough Dura mater. The network of sinuses carries venous outflow from the brain and empties into the internal jugular vein, returning the blood to the heart. Cerebral veins and sinuses are unique because, unlike other veins in the body, they do not have valves to prevent blood from flowing backward and depend on both gravity and blood pressure.

Figure 4.3. The Arterial Blood Supply of the Brain, including the Circle of Willis, as viewed from ventral surface.
V. REVIEW OF RELATED LITERATURE

A. Incidence
Stroke could soon be the most common cause of death worldwide. Stroke is currently the second leading cause of death in the Western world, ranking after heart disease and before cancer, and causes 10% of deaths worldwide. Geographic disparities in stroke incidence have been observed, including the existence of a “stroke belt” in the southeastern United States, but causes of these disparities have not been explained.
The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age. Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65. A person’s risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in childhood.
Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time. The results of this study found that the only significant genetic factor was the person’s blood type. Having had a stroke in the past greatly increases one’s risk of future strokes.
Men are 25% more likely to suffer strokes than women, yet 60% of deaths from stroke occur in women. Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002). Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).

B. Clinical Presentation and Medical Management
An ischemic stroke can cause a wide variety of neurologic deficits, depending on the location of the lesion (which vessels are obstructed), the size of the area of inadequate perfusion, and the amount of collateral (secondary or accessory) blood flow. The patient may present with any of the following signs and symptoms:
-Numbness or weakness of the face, arm, or leg, especially on ne side of the body;
-Confusion or change in mental status;
-Trouble speaking or understand speech;
-Visual disturbances;
-Difficulty walking, dizziness, or loss of balance or coordination;
-Sudden severe headache
Motor sensory, cranial nerve, cognitive and other functions may be disrupted.

Table 5-1. Neurologic Deficits of Stroke: Manifestations and Nursing Implications
Neurologic Deficit Manifestation Nursing Implication/ Patient Teaching Application Visual field deficits Homonymous hemianopsia (loss of half of the visual field) * Unaware of the persons or objects on side of the visual loss.
* Neglect of one side of the body.
* Difficulty judging distances. -Place objects within intact field of vision.
-Approach the patient from side of the intact field of vision
-Instruct/remind the patient to turn the head in the direction of visual loss to compensate for loss of visual field
-Encourage the use of eye glasses if available
-when teaching the patient, do so within the patient’s intact visual field. Loss o peripheral vision * Difficulty seeing at night
* Unaware of objects or the borders of objects -Avoid night driving or other risky activities in the darkness
-Place objects in center of patient’s intact visual field.
-Encourage the use of a cane or other object to identify objects in the periphery of visual field. Diplopia * Double of vision -Explain to the patient the location of an object when placing it near the patient.
-Consistently place patient care items in the same location. Motor Deficits Hemiparesis * Weakness of the face, arm, and leg on the same side (due to a lesion in the opposite hemisphere) -Place objects within the patient’s reach on the non affected site. Hemiplegia * Paralysis of the face, arm, and leg on the same side (due to a lesion in the opposite hemisphere) -Encourage the patient to provide range-of-motion exercises to the affected site.
-Provide immobilization as needed on the affected site.
_-Maintain body alignment in functional position.
-exercise unaffected limb to increase mobility, strength and use. Ataxia * Staggering, unsteady gait
* Unable to keep feet together; needs a broad base to stand -Support patient during the initial ambulation phase
-Provide supportive device for ambulation (walker, cane).
Instruct the patient not to walk without assistance or supporting device. Dysarthria * Difficulty in forming words -Provide the patient with alternative methods of communicating.
-Allow the patient sufficient time to respond to verbal communication.
-Support patient and family to alleviate frustration relate to difficulty communicating. Dysphagia * Difficulty swallowing -Test the patient’s pharyngeal reflexes before offering food or fluids.
-Assist the patient with meals.
-Place food on the affected site of the mouth.
-Allow ample time to eat. Sensory deficit Paresthesia (occurs on the site opposite to the lesion) * Numbness and tingling of extremity
* Difficulty with proprioception -Instruct the patient to avoid using this extremity as the dominant limb due to altered sensation.
-Provide range of motion to affected areas and apply corrective devices as needed. Verbal deficits Expressive aphasia * Unable to form words that are understandable; may be able to speak in single word responses
-Encourage patient to repeat sounds of the alphabet. Receptive aphasia * Unable to comprehend the spoken word; can speak but may not make sense. -Speak slowly and clearly to assist the patient in forming sounds. Global (mixed) aphasia * Combination of both receptive and expressive aphasia -Speak clearly and in simple sentences; use gestures or pictures when able.
-Establish alternative means of communication. Cognitive Deficits * Short and long term memory loss
* Decreased attention span
* Impaired ability to concentrate
* Poor abstract reasoning
* Altered judgment -Reorient patient to time, place and situation frequently.
-Use verbal and auditory cues to orient patient.
Provide familiar objects ( family photographs, favorite objects)
-Use no complicated language.
-Match visual tasks with a verbal cue; holding a toothbrush, stimulate brushing of teeth while saying, “I would like you to brush your teeth now.)
-Minimize distracting noises and views when teaching the patient.
-Repeat and reinforce instructions frequently. Emotional Deficits * Loss of self control
* Emotional lability
* Decreased tolerance to stressful situations
* Depression
* Withdrawal
* Fear, hostility, and anger
* Feelings of isolation -Support patient during uncontrollable outbursts.
-Discuss with the patient and family that the outbursts are due to the disease process.
-Encourage the patient to participate in group activity.
-Provide stimulation for the patient.
-Control stressful situations, if possible.
-Provide a safe environment.
-Encourage patient to express feelings and frustrations related to disease process.

C. Laboratory and Radiologic Examination
Any patient with neurologic deficits needs a careful history and a complete physical and neurologic examination. Initial assessment will focus on airway patency, which may be compromised by loss of gag or cough reflexes and altered respiratory pattern; cardiovascular status (including blood pressure, cardiac rhythm and rate, carotid bruit), and gross neurologic losses.
Stroke patients may present to the acute care facility at any point along a continuum of neurologic involvement. A system that uses the time course to classify patients along this continuum may be used to guide treatment. Strokes use the time course is commonly classified in the following manner: (1) transient ischemic attack; (2) reversible ischemic neurologic disease; (3) stroke in involution; and (4) compensated stroke.
The initial diagnostic test for a stroke is a non contrast computed therapy (CT) scan performed emergently to determine of the event is ischemic or hemorrhagic (which determines treatment). Further diagnostic work up for ischemic stroke involves attempting to identify the source of thrombi or emboli. A 12-lead electrocardiogram and a carotid ultrasound are standard tests. Other studies may include Cerebral Angiography, transcranial flow studies, transthoracic or transesophagel echocardiography, magnetic resonance imaging of the brain and/or neck, xenon CT, and single photon emission CT.
Remarkable advances in technology now make it possible to examine how the brain looks, works and gets its blood supply. These tests can outline the affected part of the brain and help define the problem created by stroke. Most of these tests are safe, painless and can be done as an outpatient. However, in many cases these tests are ordered when a patient is hospitalized with a stroke. A doctor must decide on a case-by-case basis whether such tests will be useful, and if so, which ones to use. The following tests are described in this section:
i. Carotid phonoangiography
ii. Computerized axial tomographic scan (CT or CAT scan)
iii. Digital subtraction angiography (DSA)
iv. Doppler ultrasound test
v. Electroencephalogram (EEG)
vi. Evoked response test
vii. Magnetic resonance imaging scanning (MRI)
viii. Radionuclide angiography
What imaging tests are done on the brain?
* Computerized axial tomographic scan (CT or CAT scan) – Uses X-rays to generate an image of the brain. Doctors use CT to determine whether a stroke has occurred and, if so, what kind. (Ischemic strokes are caused by a clot that blocks an artery. Hemorrhagic strokes result from a ruptured blood vessel in the brain causing bleeding into brain tissue.) CT scanning takes from 5 to 10 minutes to complete (mostly less than 5 minutes). The test causes no discomfort.
* Magnetic resonance imaging scanning (MRI) – The stroke patient is placed into the MRI scanner. This scanner has a magnetic field in which the head is subjected to bursts of energy of a known magnetic frequency. The response of the brain cells to these bursts of energy is detected as signals that ultimately generate an image of the brain. MRI can give very accurate images of the brain. These are used to determine the presence, location and size of aneurysms and arteriovenous malformations, which are potential sources for hemorrhagic stroke. This test is performed in 40 minutes to one hour, and causes no discomfort.
* Radionuclide angiography – Radioactive compounds are injected into a vein in the arm; the bloodstream then carries them toward the head. As the radioactive compound circulates in the bloodstream, it constantly emits bursts of radiation. Once the radioactive compound reaches the brain, these bursts of radiation are detected and used to form an image of the brain. This imaging procedure can show areas where the brain has been deprived of blood flow and is damaged.
What tests show the brain’s electrical activity?
* Electroencephalogram (EEG) – Small metal disks (electrodes) are placed at strategic locations on a person’s scalp. The electrodes can detect the electrical activity in the form of impulses that are then transcribed to paper. By observing such impulse characteristics as intensity (the size of the impulse), duration (the width of the impulse), frequency (how often impulses occur during a given time) and location (what region of the brain produces these impulses), an EEG can provide valuable information about underlying problems in the brain. Some people who have strokes are prone to seizures, and this test will help doctors determine if seizures are present and if treatment with medications is needed.
* Evoked response test – a diagnostic procedure that provides a measurement of the brain’s ability to process and react to different sensory stimuli. A doctor evokes a visual response by flashing a light or checkerboard pattern in front of a patient. For auditory evoked responses, a doctor produces a sound in one of the patient’s ears. For bodily evoked responses, one of the nerves in an arm or leg is electrically stimulated. The responses from these sensory stimuli can indicate abnormal areas of the brain.
What tests show blood flow?
* Doppler ultrasound test – Uses high-frequency sound waves to detect blockages in the carotid artery. A Doppler probe or instrument capable of generating ultrasound waves is placed on the neck very near to the carotid artery. Ultrasound waves from the probe travel through the neck and bounce off the moving blood cells. The reflected sound wave, now returning to the probe at a different frequency, is then detected by the same probe. The change in frequency of the sound waves relates to the speed of the blood cells and thus the blood flow. This test takes an hour or more, and causes no discomfort.
* Carotid phonoangiography – a sensitive microphone is placed on the neck, very close to the carotid artery, to record sounds. Ordinarily, in a normal artery, blood flows in a smooth and controlled manner. However, the presence of blockages, such as those caused by atherosclerosis, causes the blood flow to become turbulent. This turbulent blood flow can create a sound, called a bruit (BROO’e), which can be detected and registered by the microphone. The presence of a bruit may indicate a blockage in the carotid artery and is cause for more tests.
* Digital subtraction angiography (DSA) – gives an image of the brain’s major blood vessels. A thin plastic tube (a catheter) is inserted into a major artery of the leg and advanced through the body’s major vessels until it reaches the brain’s blood vessels. A contrast dye is injected through the catheter and allowed to circulate in the bloodstream. At that point, an X-ray machine quickly takes a series of pictures of the head and neck. The images track the movement of the contrast dye as it moves through the brain’s blood vessels. This imaging technique lets the doctor identify and localize the source of a blocked blood vessel that caused the stroke. Some people may feel a warm sensation as the contrast medium is injected into the blood vessels.
In patient with TIA, a bruit (abnormal sound heard on auscultation resulting from interference with normal blood flow) may be heard over the carotid artery. There are diminished or absent of carotid pulsationsin the neck. Diagnostic tests for TIA may include carotid phonoangiography; this involves auscultation, direct visualization, and photographic recording of carotid bruits. Oculoplethysmography measures the pulsation of blood flow through the ophthalmic artery. Carotid angiography allows visualization of intracranial and cervical vessels. Digital subtraction angiography is used to define carotid artery obstruction and provides information on patterns of cerebral blood flow.
D. NIH Stroke Scale
The National Institute of Health (NIH) stroke scale (NIHSS) is a standardized method used by physicians and other health care professionals to measure the level of impairment caused by a stroke. The NIH stroke scale serves several purposes, but its main use in clinical medicine is during the assessment of whether or not the degree of disability caused by a given stroke merits treatment with tPA. Another important use of the NIHSS is in research, where it allows for the objective comparison of efficacy across different stroke treatments and rehabilitation interventions. The NIH stroke scale measures several aspects of brain function, including consciousness, vision, sensation, movement, speech, and language. A certain number of points are given for each impairment uncovered during a focused neurological examination. A maximal score of 42 represents the most severe and devastating stroke. Current guidelines as of 2008 allow strokes with scores greater than 4 points to be treated with tPA.
Table 5-2. Summary of NIH Stroke Scale
Category
Description Score Baseline date/time Date/time 1a. Level of Consciousness (alert, drowsy, etc.)
Alert
Drowsy
Stupotous
Coma 0
1
2
3 1b. LOC questions (month, age)

Answers both correctly
Answers one correctly
incorrect 0
1
2 1c. LOC commands (open, close eyes, make fist, let go)

Obeys both correctly
Obeys one correctly
Incorrect 0
1
2 2. Best Gaze (eyes open- patient follows examiners fingers or face.
Normal
Partial Gaze Plasy
Forced Deviation 0
1
2 3. visual (introduce visual stimulus/ threat to patient’s visual field quadrants) No visual loss
Partial Hemianopia
Complete Hemianopia
Bilateral Hemianopia 0
1
2
3 4. Facial Palsy
Normal
Minor
Partial
Complete 0
1
2
3
5a. Motor arm- Left (elevate extremity to 90° and score drift movement)

No drift
Drift
Can’t resist gravity
No effort Against Gravity
No movement
Amputation joint fusion (explain)
0
1
2
3
4
9 5b. Motor arm- Right
(elevate extremity to 90° and score drift movement)

No drift
Drift
Can’t resist gravity
No effort Against Gravity
No movement
Amputation joint fusion (explain) 0
1
2
3
4
9 6a. Motor leg-Left (elevate extremity to 30° and score drift movement)
No drift
Drift
Can’t resist gravity
No effort Against Gravity
No movement
Amputation joint fusion (explain) 0
1
2
3
4
9 6b. Motor leg-Right (elevate extremity to 30° and score drift movement)
No drift
Drift
Can’t resist gravity
No effort Against Gravity
No movement
Amputation joint fusion (explain) 0
1
2
3
4
9 7. Limb ataxia (finger-to-nose and heel-to-shin testing) Absent
Present in One Limb
Present in Two Limbs 0
1
2 8. Sensory (pin prick to face, arm, trunk and leg-compare side to side)

Normal
Partial Loss
Severe Loss 0
1
2 9. Best Language (name items, describe a picture and read sentences)

No Aphasia
Mild to Moderate Aphasia
Severe Aphasia
Mute 0
1
2
3 10. Dysarthria (evaluate speech clarity by patient repeating words.) Normal Articulation
Mild to Moderate Dysarthria
Near to Unintelligible or Worse
Intubated or Other Physical Barrier 0
1
2
9 11. Extinction and Inattention (use information from LOC and motor testing to identify neglect No Neglect
Partial Neglect
Complete Neglect 0
1
2 ________________________________________________________________________ Individual Administering Scale: The level of stroke severity as measured by the NIH stroke scale scoring system:
0 = no stroke
1-4 = minor stroke
5-15 = moderate stroke
15-20 = moderate/severe stroke
21-42 = severe stroke

VI. PATHOPHYSIOLOGY

In an ischemic brain attack, there is disruption of the cerebral blood flow due to obstruction of blood vessel. This disruption in blood flow initiates a complex series of cellular metabolic events referred to as the ischemic cascade.
The ischemic cascade begins when cerebral blood flow falls less than 25 ml/100 g/min. at this point, neurons can no longer maintain anaerobic respiration. The mitochondria must then switch to anaerobic respiration, which generates large amounts of lactic acid, causing a change in pH level. This switch to the less efficient anaerobic respiration also renders the neuron incapable of producing sufficient quantities of adenosine triphosphate (ATP) to fuel the depolarization process. Thus membrane pumps that maintain electrolyte balances begin to fail and the cells cease to function.
Early in the cascade, an area of low cerebral blood flow, referred to as penumbra region, exists around the area of infarction. The penumbra region is ischemic brain tissue that can be salvaged with timely intervention. The ischemic cascade threatens cells in the penumbra because membrane depolarization of the cell walls leads to an increase in intracellar calcium and the release of glutamate. The penumbra area can be revitalized with the administration of tissue plaminogen activator (t-PA), and the influx of calcium can be limited with the use of cacium channel blocker. The influx of calcium and release of glutamate, if continued, activate a number of damaging pathways that result in the destruction of the cell membrane, the release of more calcium and glutamate, vasoconstriction, and the generation of free radicals. These processes enlarge the area of infarction into the penumbra, extending the stroke.

Figure 6-1. Pathophysiology of the Cerebrovacular Accident. Process contributing to ischemic brain iinjury. Courtesy of National Stroke Association, Englewood, Colorado
VII. LABORATORY RESULTS

A. Complete Blood Count

Dec 06 2010 Normal values Interpretation Hemoglobin 117 g/L 123-152 g/ L Lower Hematocrit 0.36 0.37-0.42 % Slightly lower WBC count 11.9 5.0-10.0 x 10 g/L Higher Differential Count Lymphocytes 0.22 0.20-0.40 Normal Monocytes 0.07 0.02-0.08 Normal Eosinophils 0.01 0.01-0.03 Normal Basophils 0.01 0-0.02 Normal Neutrophils 0.69 0.40-0.60 Higher RBC 4.98 4.5-5.5×10/2 L Normal MCV 73 88-96 Lower MCH 23.5 27-33 pg Lower MCHC 321 330-360 g/L Lower RDW 14.3 12.7-22.7 % Normal Platelet 210 150-450x 10 g/L Normal MPV 9.47 4.5-7.5 Higher PDW 3.17-39.1 CT 2-4 mins. BT 1-3 mins. Reticular Count 05-1.5% ESR 0-20 mm/hr
B. Electrolytes

Creatinine 88.2mmol/L Sodium 135 mmol/L Potassium 4.3 mmol/L Calcium 1.12 mmol/L Chloride 92 mmol/L
C. Clinical Chemistry
Cholesterol 5.0 mmol/L Triglycerides 0.32 mmol/L Didevet HDL Cholesterol 1.9 mmol/L LDL Cholesterol 3.66 mmol/L
D. CT Scan
December 7 2010:
Impression: Cortical cerebral atrophy.

E. CT Scan: Cervical Spine with settings for the soft tissues and bone detail revealed.
December 7 2010
Findings:
-Scannogram shows mild reversal of the cervical lordesis most likely due to muscular spasm.
-Thecal sac is intact.
-There is no evidence of canal stenosis
-Osteophytic formation is ruled at C5 and C6 vertebral bodies.
-Visualized soft tissue planes within normal.
-No other findings noted.
VIII. PHARMACOLOGY

A. Mannitol

Brand name Osmitrol Patient’s Dosage 75 mg prn Classification Diagnostic agent; osmotic diuretic, urinary irrigant Indication * Prevention and treatment of oliguric phase of renal disease
* Reduction of intracranial pressure and treatment of cerebral edema; of elevated IOP when the pressure cannot be lowered by other means
* Promotion of the urinary excretion of toxic substances
* Diagnostic use: measurement of GFR
* Irrigant in transurethral prostatic resection or other transurethral precedures Action Elevates the osmolarity of the glomerular filtrate, thereby hindering the reabsorption of water and leading to a loss of water, sodium, chloride (used for diagnosis of glumerular filtration rate); creates an osmotic gradient in the eye between plasma and oclular fluids, thereby reducing IOP; creates an osmotic effect, leading to decreased swelling in posttransurethral prostatic resection. Pharmacokinetics Route Onset Peak Duration IV
Irrigant 30-60 minutes
Rapid 1 hour
Rapid 6-8 hours
Short Metabolism T 1/2 : 15-100 minutes Distribution Crosses placenta; may enter breast milk Excretion Urine Dosage and Administration Adults:
IV infusion only; individualized concentration and rate of administration. Dosage is 50-200g/day. Adjust dosage to maintain urine flow of 30-50 ml/hr.
* Prevention of oliguria: 50-100 g IV as a 5% -25% solution
* Treatment of oliguria: 50-100 g IV of a 15%-25% solution.
* Reduction of intracranial pressure and cerebral edema: 1.5-2g/kg IV as a 15%-25% solution over 30-60 minutes. Evidence of reduced pressure should be seen in 15 minutes.
* Reduction of IOP: infuse 1.5-2 g/kg as a 25% solution, 20% solution. Or 15% solution over 30 minutes. If used preoperatively, use 60-90 minutes before surgery for maximal effect.
* Adjunctive therapy to promote dieresis in intoxications: maximum of 200 g IV of mannitol with other fluids and electrolytes.
* Measurement of glumerular filtration rate: dilute 100 ml of a 20% solution with 108 ml of sodium chloride injection. Infuse this 280 ml of 702% solution IV at rate of 20 ml/ min. collect urine with a catheter for the specified time for measurement of mannitol in mg/min. draw blood at the start and at the end of the time for measurement of mannitol in mg/ml plasma.
* Test dose of mannitol for patients with inadequate renal function: 0.2 g/kg IV (about 50 ml of 25% solution, 75 ml of a 20% solution) in 3-5 minutes to produce urine flow of 30-50 ml/hour. If urine flow does not increase, repeat dose. If no response to second dose, reevaluate patient situation.
* Urologic irrigation: use prepared 5g/ 100ml distilled water solution; irrigate as needed.
Pediatric patients:
Dosage for children younger than 12 yr not established. Contraindications Contraindicated with anuria due to severe renal disease Precaution Use cautiously with pulmonary congestion, active intracranial bleeding (except during crainiotomy), dehydration, renal disease, heart failure, pregnancy, lactation. Adverse Reactions and Side effects Central Nervous System Dizziness, headache, blurred vision, seizzures Cardiovascular Hypotension, hypertension, edema, HF, thromboplebitis, tachycardia, chest pain Dermatologic Urticaria, skin necrosis with infiltration Gastrointestinal Nausea, anorexia, dry mouth, thirst Genitourinary Diuresis, urine retention Hematologic Fluid and electrolyte imbalances Respiratory Pulmonary congestion, rhinitis Nursing Considerations Assessment * History Pulmonary congestion, active intracranial bleeding, dehydration, renal disease, heart failure, pregnancy, lactation
* Physical Skin color, lesions, edema, hydration, orientation, muscle strength , reflexes, pupils, pulses, BP, perfusion; Respiratory pattern, adventitious sounds, urinary output patterns, serum electrolytes, urinalysis , renal function tests Interventions Warning: Do not give electrolyte free mannitol with blood. If blood must be given, add at least 20 mEq of sodium chloride to each liter of mannitol solution
* Do not exposesolutions to low temperatures; crystallization may occur. If crystals are seen, warm the bottle in a hot water bath, then cool to body tempearature before administering.
* Make sure the infusion set contains a filter if giving concentrated mannitol.
* Monitor serum electrolyte periodically with prolonged therapy. Teaching Points * You may experience these side effects: Increased urination; GI upset (eat frequent small meals); dry mouth (suck sugarless lozenges); headache, blurred vision (use caution when moving for assistance).
* Report difficulty of breathing, pain in the IV site, chest pain.
B. Tramadol hydrochloride

Brand name Ultral, Ultral ER Patient’s Dosage 50 mg PO q 6h Classification Analgesic (centrally acting)
Opoid Analgesic Indication * relief of moderate to moderately severe pain
* relief of moderate to severe chronic pain
in adults who need RTC Treatment for extended periods (ER tablets)
* Unlabelled uses: Premature ejaculation; restless leg syndrome
Action Binds to mu-opiod receptors and inhibits the reuptake of norepinephrine and serotonin; causes many effects similar to opoids- dizziness, somnolence, nausea, constipation – but does not have the respiratory depressant effects. Pharmacokinetics Route Onset Peak Oral 1 hour 2 hours Metabolism Hepatic; t 1/2 : 6-7 hours Distribution Crosses placenta; enters breast milk Excretion Urine Dosage and Administration Adults:
* Patients who require rapid analgesic effect: 50-100mg PO every 4-6 hr; do not exceed 400 mg/day
* Patients with moderate to moderately severe chronic pain: Initiate at 25 mg /day in the morning, and titrate in 25-mg increments every 3 days to reach 100 mg/day. Then increase every 3 days to reach 200 mg/day. After titration, 50-100mg every 4-6 hours; do not exceed 400 mg/day. Alternatively, 100-mg ER tablet once daily, titrated by 100-mg increments every 5 days; do not exceed 300 mg/day.

Pediatric Patients
Safety and efficacy not established.

Geriatric Patients or patients with hepatic or renal impairment
Older than 75 years old: do not exceed 300 mg/day
Patients with cirrhosis: 50 mg every 12 hour ER tablets should not be used in severe hepatic impairment
Patients with creatinine clearance less than 30ml/min: 50-100 mg PO every 12 hours. Maximum 200 mg/day. ER tablets should not be used in patients with creatinine clearance less than 30 ml/min.
Contraindications Contraindicated with allergy to tramadol, or opoids or acute intoxication with alcohol opoids and psychoactive drugs. Precaution Use cautiously with pregnancy, lactation; seizures; concomitant use of CNS depressants, MAOIs, SSRIs, TCAs; renal impairment; hepatic impairment. Adverse Reactions and Side effects Central Nervous System Sedation, dizziness or vertigo, headache, confusion, dreaming, sweating, anxiety, seizures Cardiovascular Hypotension, tachycardia, bradycardia Dermatologic Sweating, pruritus, rash, pallor, urticaria Gastrointestinal Nausea, vomiting, dry mouth, constipation, flatulence Others Potential abuse, anaphylatoid reactions Drug Interactions * Devreased effectiveness with carbamazepine
* Increased risk of tramadol toxicity with MAOIs or SSRIs Nursing Considerations Assessment * History
Hypersensitivity to tramadol; pregnancy; acute intoxication with alcohol, opoids, psychotropic drugs or other centrally acting analgesics; lactation; seizures; concomitant use of CNS depressants or MAOIs; renal ore hepatic impairment; past or present history of opoid addiction
* Physical Skin color, texture, lesions; orientation, reflexes, bilateral grip strength, affect; Pulmonary auscultation, BP; bowel sounds, normal output; LFTs, renal function tests Interventions * Control environment (temperature, lighting,) if sweating or CNS effects occur.
Warning: Limit use in patients with past or present history of addiction to or dependence on opoids. Teaching points * You may experience these side effects: dizziness, sedation, drowsiness, impaired visual acuity (avoid driving or performing tasks that require alertness); nausea, loss of appetite, (lie quietly, eat frequent small meals)
* Repot severe nausea, dizziness, severe constipation.
C. Celecoxib

Brand name Celebex Patient’s Dosage 100 mg PO bid Classification Analgesic (nonopoid)
NSAID
Specific COX-2 enzyme inhibitor Indication * acute and long term treatment of Signs and symptoms of rheumatoid arthritis and osteoarthritis
* reduction of the number of colorectal polyps in familial adenomatous polyposis (FAP)
* management acute pain
* treatment of primary dysmenorrhea
* relief of signs and symptoms of ankylosing spondylitis
* Relief of signs and symptoms of juvenile rheumatoid arthritis. Action Analgesic and anti-inflammatory activities related to inhibition of the COX-2 enzyme, which is activated I inflammation to cause the signs and symptoms associated with inflammation; does not affect the COX-1 enzyme, which protects the lining of the GI tract and has blood clotting and renal functions. Pharmacokinetics Route Onset Peak Oral Slow 3 hours Metabolism Hepatic; t 1/2 : 11 hours Distribution Crosses placenta; may enter breast milk Excretion Bile, urine Dosage and Administration Adults
Initially, 100mg PO bid; may increase to 200 mg/day PO bid as needed.
* acute pain, dysmenorrheal: 400mg, then 200mg PO bid
* FAP: 400mg PO bid
* Anyklosing spondylitis: 200mg/day PO; after 6week,; if no effect, suggest another therapy.

Pediatric Patients
10 kg or 25 kg or less: 50 mg capsule PO bid.
More than 25 kg: 100 mg capsule PO bid. Contraindications Contraindicated with allergies to sulfonamides, celecoxib, NSAID’s or aspirin; significant renal impairment; pregnancy (third trimester), lactation. Precaution Use cautiously with impaired hearing, hepatic and CV condition. Adverse Reactions and Side effects Central Nervous System Headache, dizziness, somnolence, insomnia, fatigue, tiredness, dizziness, tinnitus, ophthalmologic effects Cardiovascular MI, CVA Dermatologic Rash, pruritis, sweating, dry mucous membranes, stomatitis Gastrointestinal Nausea, abdominal pain, dyspepsia, flatulence, GI bleed Hematologic Neutropenia, eosinophilia, leucopenia, pancytopenia, thrombocytopenia, agranulocytosis, granulocytopenia, aplastic anemia, decreased Hgb or Hct, bone marrow depression, menorrhagia Others Peripheral edema, anaphylactoid reactions to anaphylactic shock Drug Interactions * Increased risk of bleeding if taken concurrently with warfarin. Monitor patient closely and reduce warfarin dose as appropriate.
* Increased lithium level and toxicity.
* Increased risk of GI bleeding with long term use of alcohol, smoking. Nursing Considerations Assessment * History Renal impairment, impaired hearing, allergies hepatic and CV conditions, lactation and pregnancy.
* Physical Skin color and lesions; orientation, reflexes, ophthalmologic and audiometric evaluation, peripheral sensation; Pulmonary edema, Respiratory, adventitious sounds; liver evaluation; CBC, LFT’s, renal function tests; serum electrolytes. Interventions Block Box warning: Be aware that the patient maybe at increased risk for CV events, GI Bleeding; monitor accordingly.
* Administer drug with food or after meals if GI upset occurs.
* Establish safety measures if CNS or visual disturbances occur.
* Arrange for periodic ophthalmologic examination during long term therapy.
Warning: If overdose occurs, institute emergency procedures-gastric lavage, induction of emesis, supportive therapy.
* Provide further comfort measures to reduce pain (e.g. positioning, environmental control) and t reduce inflammation (e.g. warmth, positioning, and rest). Client/ Family Teaching * Take only the prescribed dosage, do not increase dosage.
* You may experience these side effects: Dizziness, drowsiness (avoid driving or the use of dangerous machinery while taking this drug).
* Report sore throat, fever, rash, itching, swelling in ankles or fingers; changes in vision.
D. Olmesartan medoxomil

Brand name Benicar Patient’s Dosage 20 mg/ day PO as a once-daily dose Classification Angiotensin II receptor antagonist
Antihypertensive Indication Treatment of hypertension, alone or in combination with other hypertensives. Action Selectively blocks the binding Angiotensin II to specific tissue receptors found in the vascular smooth muscle and adrenal gland; this action blocks the vasoconstricting effect of the renin-angiotensin system as well as the release of aldosterone leading to decreased BP; may prevent the vessel remodeling associated with the development of atherosclerosis. Pharmacokinetics Route Onset Peak Oral Varies 1-2 hours Metabolism Hydrolyzed in GI tract; T 1/2 : 13hours Distribution Crosses placenta; enters breast milk Excretion Feces, urine Dosage and Administration Adults
20 mg/day as a once-daily dose; mat titrate to 40 mg/day if needed after 2 weeks.

Pediatric Patients
Safety and efficacy not established. Contraindications Contraindicated with hypersensitivity to any component of drug, pregnancy (use during the second or third trimester can cause injury or death to the fetus. Precaution Use cautiously with renal impairment, hypovolemia, salt depletion. Adverse Reactions and Side effects Central Nervous System Headache, dizziness, syncope, muscle weakness Cardiovascular Hypotension, tachycardia EENT Rash, inflammation, urticaria, pruritus, alopecia, dry skin Gastrointestinal Diarrhea, abdominal pain, nausea, constipation, dry mouth, dental pain Hematologic Increased CPK, hyperglycemia, hypertriglycemia Respiratory URI symptoms, bronchitis, cough, sinusitis, rhinitis, pharyngitis. Others Back pain, flulike symptoms, fatigue, hematuria, arthritis Nursing Considerations Assessment * History Hypersensitivity to any component of the drug, pregnancy, lactation, hepatic or renal impairment hypovolemia, salt depletion.
* Physical Skin lesions, turgor; body temp; reflexes, affect; BP, R, respiratory auscultation; LFTs, renal function tests, serum electrolytes. Interventions * Administer without regard to meals.
Black Box Warning: ensure that patient is not pregnant before beginning therapy. Suggest the use of barrier birth control while using olmesartan; fetal injury and deaths have been reported.
* Find an alternate method of feeding infant if given to a nursing mother. Depression of the renin-angiotensin system in infants is potentially very dangerous.
Warning: alert the surgeon and mark the patient’s chart with notice that the olmesartan is being taken. The blockage of the renin-angiotensin system following the surgery can produce problems. Hypotension may be reversed with volume expansion.
* Monitor patient closely in any situation that may lead to decreased in BP secondary to reduction in fluid volume- excessive perspiration, dehydration, vomiting, diarrhea; excessive hypotension can occur. Client/ Family Teaching * Take drug without regard of meals. Do not stop taking this drug without consulting your health care provider.
* Use barrier method of birth control while using this drug; if you become pregnant or desire to become pregnant, consult your health care provider.
* Take special precautions to maintain your fluid intake and safety precautions in any situations that night cause a loss of fluid volume-excessive perspiration, dehydration, vomiting, diarrhea; excessive hypotension can occur.
* You may experience these side effects: Dizziness (avoid driving a car or perform hazardous activitie0; headache (medications may be available to help) nausea, vomiting diarrhea (proper nutrition is important, consult dietician o maintain nutrition); symptoms of the upper respiratory tract and cough (do not self medicate, consult your health care provider if this becomes uncomfortable).
* Report fever, chills, dizziness, pregnancy, and swelling.