Chapter 47: Care Of Critically Ill With Neuro Problems Flashcards

0
Q

Stroke/brain attack

A

It is a medical emergency and should be treated immediately to prevent neurologic deficits and permanent disability. The brain cannot store oxygen or glucose and must receive a constant flow of blood. Blood is interrupted for more than a few minutes cerebral tissue dies which is called infarction. Brain metabolism and bloodflow are affected around the infarctions as well as in the contralateral side, which may be due to brain swelling. They are classified as ischemic or hemorrhagic. Ischemic strokes include thrombotic or embolic

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1
Q

TIA. Transient ischemic attack

A

Is also called a silent stroke. They cause temporary neurological dysfunction resulting from a brief interruption of cerebral blood flow usually do to cerebral vasospasm or systemic arterial hypertension. It lasts from a few minutes to less than 24 hours. It is called a reversible ischemic neurologic deficit RIND if it lasts longer than 24 hours but less than a week. Symptoms usually resolved within 30 to 60 minutes. They may damage brain tissue. They indicate high stroke risk. The patient is usually placed on anticoagulant therapies at discharge.

Symptoms include visual deficits such as blurred vision, diplopia, blindness in one eye, tunnel vision.
Motor deficits such as weakness and gate disturbance.
Sensory deficits such as numbness or vertigo. Speech deficits such as aphasia and dysarthria which is slurred speech

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2
Q

Thrombotic stroke

A

Is caused by a clot. More than half of all strokes. Usually associated with atherosclerosis of the blood vessel wall. It causes an occlusive stroke. It usually has a slow onset because of gradual occlusion.

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3
Q

Embolic stroke

A

Is caused by a dislodged clot. The emboli usually comes from the heart and travels via the carotid artery. They occur in patients with nonvalvular atrial fibrillation, ischemic heart disease, rheumatic heart disease, and after a MI. The emboli lodge in the cerebral blood vessels. The occlusion maybe temporary if it breaks into smaller fragments and is absorbed. They are characterized by sudden development of rapid occurrence of neurologic deficits. The symptoms may resolve over several hours or a few days. It could develop into a hemorrhagic stroke because of weakness in the vessel.

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4
Q

Hemorrhagic stroke

A

Bleeding occurs in the brain tissue or spaces surrounding the brain. Often from a ruptured aneurysm or arteriovenous malformation but most commonly from severe hypertension. Amphetamine abuse can cause hemorrhagic stroke. Cocaine can cause both hemorrhagic and ischemic

When an aneurysm ruptures vasospasm and constriction of the artery results and blood flow to the distal areas of the brain is diminished which leads to ischemia and infarction.

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5
Q

Aneurysm

A

Abnormal ballooning or blister along a normal artery. It can be congenital or secular which is when a really weak spot develops on the artery wall. It is often described as the worst headache of my life. Other symptoms include nausea and vomiting, photophobia, cranial neuropathy, stiff neck, the change in mental status

Dissecting
Pseudo aneurism is dilation of an artery
Mycotic from infectious agent causing endocarditis

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6
Q

AVM. ATRIAL VENOUS MALFORMATION

A

Occurs during embryonic development. A spaghetti like mass of dilated thin-walled vessels. They may eventually ruptured and cause bleeding into the brain.

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7
Q

Risk factors for stroke

A

Atrial fibrillation or heart murmur, arteriosclerosis or atherosclerosis, previous stroke, transient ischemic attack, heart surgery, valvular heart disease, diabetes mellitus, smoking, substance abuse especially cocaine, obesity, sedentary lifestyle, oral contraceptives, elevated cholesterol, Heavy alcohol use, seven discontinuation of antihypertensive drugs, genetic tendency, migraines, older age, male, African-American Hispanic or American Indian, sickle cell anemia, use of PPA which is found in antihistamines, Brain trauma

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8
Q

Assessment for a stroke

A

Must be evaluated within 10 minutes of arrival to the emergency department. Priority assessment is ABC. Performing urologic assessment. Use the NIH stroke scale. Evaluate cognitive changes and IICP.
Assess muscle tone. Proprioception, sounds coordination in gate, agnosia the ability to use an object correctly, and apraxia which is purposeful motor activity. Assess for bowel and bladder dysfunction. Assess sensory changes.

Assess visual pupil constriction or dilation, ptosis, deficits, Petechiae of the conjunctiva, blindness, hemianopsia which is blindness in half of the visual field, Nystagmus.

Cranial nerve assessment includes cranial nerve five the ability to chew, nine and 10 is the ability to swallow, seven is facial paralysis, nine is absent gag reflex, 12 is impaired tongue movement.
Perform a cardiovascular assessment. They may have extremely high blood pressure, but a blood pressure of about 150/100 is needed to maintain cerebral perfusion after a stroke.

Emotional lability may be especially if it is in the front lobe of the brain.

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9
Q

Right cerebral hemisphere stroke

A

Involve visual and spatial awareness in proprioception. They are often unaware of deficits and maybe disoriented to time and place. Personality changes include impulsivity, poor judgment. They may have impaired sense of humor, inability to recognize faces, euphoria, constant smiling, denial of illness, overestimation of abilities, loss of ability to hear variations in tone.

Often have neglect syndrome which is being unaware of the existence of his or her left side

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10
Q

Left hemisphere stroke

A

Aphasia which is the inability to use or comprehend language, Alexia or dyslexia, agraphia which is difficulty writing, and acalculia which is difficulty with calculations. They may have deficits to the right visual field, have problems discriminating words and letters. They will be slow, cautious, anxiety, depression from the illness, worries over the future, quick to anger and frustration, and have intellectual impairment. No problems with hearing

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11
Q

Increased intracranial pressure

A
10-15 mm Hg
Decreased level of consciousness
behavior changes such as restlessness, 
     irritability, and confusion 
headache 
nausea and vomiting 
change in speech pattern, aphasia, slurred      
     speech 
changes sensorimotor status
Pupillary changes dilated and nonreactive or  
       constricted and nonreactive 
cranial nerve dysfunction 
ataxia 
seizures in first 24 hrs after stroke. 
Cushing's Triad: severe hypertension, widened 
      pulse pressure, bradycardia 
abnormal posturing: decerebrate or decorticate
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12
Q

Interventions for patient with a stroke/intracranial pressure monitoring

A

The first sign of increasing pressure is a declining level of consciousness.
Assist with monitoring device insertion.
Provide information to family and significant others.
Calibrate and level the transducer.
Set alarms.
Record ICP pressure readings.
Note the patient’s changes in response to stimuli.
Monitor cerebral perfusion pressure.
Monitor the patient’s ICP and neurologic response to care activities.
Monitor intake and output.
Monitor insertion site for infection such as
temperature and wbc count.
Administer pharmacologic agents to maintain ICP within specified range.
Space nursing care to minimize ICP elevation. Notify healthcare provider if they do not respond to treatments.
Avoid hyper oxygenating the patient before suctioning. Suctioning may increase ICP. Monitor vital signs every 2 to 4 hours. Notify the doctor if BP over 150/100.

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13
Q

Hydrocephalus

A

Increased cerebral spinal fluid with in the subarachnoid or ventricular space. May occur as a result of blood in the cerebrospinal fluid. Cerebral edema and hydrocephalus is left untreated, increased ICP results. Manifestations include increased intracranial pressure, changes in level of consciousness, headache, pupil changes, seizures, poor coordination, behavior changes.

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14
Q

Expressive aphasia/Broca’s or motor

A

Is the result of damage in the Brokas area of the frontal lobe. It is a motor speech problem in which the patient generally understands what is said but cannot communicate verbally. They may also have difficulty writing. often autonomic speech such as responses to a greeting is not affected. The patient is aware and may become angry or frustrated. Reassure and remind them to talk slowly

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15
Q

Receptive aphasia/Wernecke’s or sensory

A

Injury involving the Wernicke’s area in the temporoparietal area. The patient cannot understand the spoken and written word. They may be able to talk but the language is often meaningless. Neologisms which are made up words are common parts of speech.

16
Q

Bladder retraining

A

Offer the bedpan or commode every two hours. Increase fluids to at least 2000 mL daily. Check the bladder with the ultrasound for residual urine.

Determine the reason for incontinence such as an altered level of consciousness, impaired innervation, or inability to communicate.

17
Q

Manifestations of a traumatic brain injury

A

Cluster of symptoms is called postconcussion syndrome. Amnesia, seizure, loss of consciousness, sleepiness, restlessness, irritability, disorientation, skull bruising and tenderness, personality changes, diplopia, gate changes.
Severe head injury includes pupil changes, bradycardia, papilledema, High blood pressure with a widened pulled pressure, hypertension and tachycardia if they have a hypovolemic shock, nuchal rigidity from a cerebrospinal fluid leak

18
Q

Basilar skull fracture

A

Occurs at the base of the skull, usually extending into the anterior, middle, or posterior fossa and results in cerebrospinal fluid leakage from the nose or ears. It has a potential for hemorrhage caused by damage to the internal carotid artery. Cranial nerves I II VII and VIII are damaged. Possible infection.

19
Q

Pathophysiology of increased intracranial pressure

A

Occurs when the brain cannot accommodate further volume changes. As pressure increases, cerebral perfusion decreases, leading to tissue hypoxia, a decrease in serum pH level, and an increase in the level of carbon dioxide. This process causes cerebral vasodilation, edema, and a further increase in intracranial pressure. The cycle continues.

If it remains untreated the brain may herniate downward toward the brainstem or laterally from a unilateral lesion causing irreversible brain damage and possibly death. This is called brain herniation syndrome.

20
Q

Temporal bone fracture/Epidural hematoma

A

Often causes an epidural hematoma which is an arterial bleed into the space between the Dura and inner skull. They have a lucid interval intervals the last for minutes during which time the patient is awake and talking. Followed by moments of unconsciousness that occurs within minutes after the injury. Symptoms progressed quickly with potentially catastrophic ICP elevation and structural changes. Symptoms increase, they lose consciousness comment and become increasingly unstable. It is a neurosurgical emergency

21
Q

Brain herniation

A

The brain may shift and herniate downward as a result of increased pressure.

Uncal herniation is a shift of the temporal lobe. It creates pressure on the third cranial nerve. Findings include dilated and nonreactive pupils, ptosis, and rapidly deteriorating level of consciousness.

Central herniation is caused by a downward shift of the brainstem in the diencephalon. It is manifested by Cheyne-Stokes respirations, pinpoint and nonreactive pupils, hemodynamic instability.

22
Q

Oxygenation for the intubated patient with a head injury

A

Carefully observe increased intracranial pressure if suctioning. Overly aggressive hyperventilation with suctioning maybe dangerous because of the cerebrovascular constriction caused by transient hypocapnia. This may increase the risk of cerebral ischemia. Allow the patient to rest between passes.

23
Q

Osmitrol/mannitol

A

And osmotic diuretic used to treat cerebral edema by pulling water out of the extracellular space of the swollen brain tissue. Is more effective when given in boluses. Administered through a filter in the IV tubing or if given by IV push draw up with a filtered needle to eliminate microscopic crystals. Monitor intake and out put, dehydration, signs of renal failure, Weakness, edema, and changes in urine output. Monitor electrolyte levels every six hours. Try to obtain a serum osmolarity of 310-320. Use a urinary catheter for strict measurement of output.

24
Q

Drug-induced coma/barbiturate coma

A

Is used for intracranial hypertension/increased ICP that cannot be controlled by other means. Either pentobarbital sodium or thiopentone is the drug of choice. They decrease the metabolic demands of the brain in cerebral blood flow, stabilize cell membranes, decrease the formation of vasogenic edema, and produce a more uniform blood supply. It is difficult to recognize neurological changes. The patient required mechanical ventilation, hemodynamic monitoring, and intracranial pressure monitoring. Complications include decreased G.I. motility, cardiac dysrhythmias from hypokalemia, hypotension, and fluctuations in body temperature.