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Neurological Alterations Study Guide for Exam Dr. Kelly Allred...

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Neuro Study Guide 1. How does LOC relate to Cerebral Blood Flow? How do you assess CBF? Cerebral Blood Flow •

15% of total cardiac output

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Brain uses 20% of O2 and 25% of glucose

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Factors influencing CBF •

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CO2 •

Increased: relaxes smooth muscles, dilates cerebral vessels, decreases cerebrovascular resistance, increases CBF

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Decreased: constrict cerebral vessels, increases cerebrovascular resistance, decreases CBF

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Less than 50 mmHg results in cerebrovascular dilation, decreases cerebrovascular resistance, increases CBF, increases oxygen tension

O2

Hydrogen Ion Concentration •

If oxygen tension is not increased lactic acidosis  vasodilation  loss of autoregulation

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Level of consciousness (LOC) is most sensitive indicator of neurologic function to impaired CBF

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Change in LOC can be subtle or dramatic •

Related to decreased blood flow to RAS (maintain wakefulness)

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Flattening of affect  change in orientation  decreased attention  coma

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Coma: No response to painful stimuli, absent corneal & pupillary reflexes, incontinent, unable to swallow and cough

Glasgow Coma Scale •

Ability to speak

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Obey commands

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Open eyes to verbal or painful stimulus

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Gold standard to assess LOC

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Score range from 3-15; lower the score, higher severity of injury and lower level of brain functioning

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GCS of 8: coma

2. Clinical manifestations of increased ICP. What are the normal values? How will you know if the patient’s ICP is increasing? What will happen? Increases Cranial Pressure Clinical Manifestations: •

Changes in vital signs (Cushing’s, temperature)

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Ocular signs: anisocoria, ipsilateral dilation, if fixed & dilated is an emergency (indicates herniation)

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Headache: continuous, worse in mornings

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Vomiting: not preceded by nausea, projectile

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Decreased motor function: contralateral hemiparesis or hemiplegia •

posturing (decorticate or decerebrate)

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Decorticate: flexion of arms, extension and internal rotation of legs

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Decerebrate: arms and legs extended with wrists flexed

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Flaccid

Factors that influence ICP      

Arterial pressure Venous pressure Intraabdominal and intrathoracic pressure Posture Temperature Blood gases (CO2 levels)

Regulation and Maintenance •

Monro-Kellie doctrine •

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Normal ICP 5 to 15 mm Hg •

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If one component increases, another must decrease to maintain ICP

Elevated if >20 mm Hg sustained **Must be treated!

Autoregulation •

Adjusts diameter of blood vessels

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Ensures consistent CBF

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Only effective if mean arterial pressure (MAP) 70 to 150 mm Hg

The Monro-Kellie doctrine states that the three components must remain at a relatively constant volume within the closed skull structure. If the volume of any one of the three components increases within the cranial vault and the volume from another component is displaced, the total intracranial volume will not change. •

This hypothesis is only applicable in situations in which the skull is closed.

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The hypothesis is not valid in persons with displaced skull fractures or hemicranectomy.

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ICP can be measured in the ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer.

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Normal intracranial ICP ranges from 5 to 15 mm Hg. A sustained pressure greater than 20 mm Hg is considered abnormal and must be treated.

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ICP can increase d/t increased

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Brain tissue volume – cerebral edema, mass

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CSF – hydrocephalus

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Blood – vasodilation

↑ ICP results in hypercapnia, cerebral acidosis, impaired autoregulation, systemic hypotension, cerebral edema, further increases ICP

3. What is CPP? What happens when there is inadequate CPP? What are the nursing interventions that can improve CPP? MAP – ICP = CPP •

Normal range = 60 – 100 mmHg

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50 mmHg will maintain only basic cerebral functioning

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< 30 mmHg = Ischemia and incompatible with life

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Loss of autoregulation = ↑ SBP to attempt to ↑ CPP

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Cushing’s Triad: 1.Systolic hypertension with widening pulse pressure, 2. Bradycardia with full bounding pulse, 3. Altered respirations (Neurological emergency)

4. What is herniation? What are the clinical manifestations of it? ICP Complications •

Inadequate cerebral perfusion

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Herniation

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Falx cerebri

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Tentorium cerebelli

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Tentorial herniation (central herniation): downward foramen magnum

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Uncal herniation: lateral and downward herniation

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Cingular herniation: lateral displacement beneath falx cerebri

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Most common traumatic herniation is uncal herniation (transtentorial herniation)

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The uncus is compressed & cranial nerve III is compressed

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First signs include anisocoria, ptosis, impaired extraocular movements, and a sluggish pupillary light reflex ipsilateral to the expanding mass lesion

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As the compression progresses, the ipsilateral pupil dilates and becomes nonreactive

Six (dilated) and fixed (atropine can cause this so beware of what meds they are on)

5. What complications can occur with ICP monitoring? Pressure devise for monitoring can be placed in the epidural, subdural, subarachnoid, parenchymal, or ventricular areas Easiest is putting a bolt in the subarachnoid space. Bacitracin q8h and watch the monitoring for pressure between 5-15

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Maintain adequate CPP and oxygenation

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Avoid secondary injury while the brain recovers

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Drawbacks: infection risk, hemorrhage, cost

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Keep ICP less than 20 mmHg

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CSF production 20-30mL/hr with total CSF 90-150mL in ventricles & subarachnoid spaces

6.         

What are the nursing interventions for ICP monitoring? Intubation, ventilation ( to give the body a break from breathing) Supplemental oxygen (PaO2 > 100mmHg) ICP monitoring Head elevation: 30 degrees neutral position Maintenance of fluid balance, check osmolality Serum Osmo 300-320mOsm/L Promotion of CPP > 60mmHg (adequate BP) Reduce cerebral metabolism (barbiturates) Removal source of increased ICP

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Decrease brain fluid volume o

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Osmotic diuretics (mannitol, hypertonic saline – 3% NS) 

Want to pull fluid back into the vessels

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Drawback of mannitol: must be given with another diuretic to have the kidneys flush it out so it doesn’t flow back into the tissues.

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Loop diuretics (furosemide)

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Corticosteroids (dexamethasone) in brain tumors/ bacterial meningitis

Decrease cerebral metabolism o

High-dose barbiturates (pentobarbital)

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Propofol (Diprivan) – sedation 

To give brain a rest

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Antiseizure drugs

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Peptic ulcer prevention (stress ulcers) with PPI (pantoprazole) or H2-receptor antagonists (cimetidine)

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Maintain SBP above 100mmHg (100-160) or MAP above 65

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Nutritional initial replacement after 3rd day of injury

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Normal saline is preferred to avoid decrease in serum osmolality and increase cerebral edema

Nursing Management of ICP •

Maintain respiratory function •

Patent airway- position head appropriately

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Suction only as needed because any suctioning can increase ICP

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Head elevation (no higher than 30 degrees)

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Monitor ABGs

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Avoid abdominal distention, noxious stimulim (when you increase intra-abdominal pressure, it increases your intra-thoracic pressure which will decrease your cardiac output)

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Treat pain, anxiety

Control body temperature •

Hyperthermia is damaging to brain

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Hypothermia may be protective

Nutrition •

Nutritional needs often increased; patient cannot meet needs

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Enteral feeding tube or TPN

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Monitor ICP or neurologic function

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Maintain fluid and electrolyte balance

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Provide adequate hydration

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Monitor intake

Monitor urinary output and volume status •

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Monitor electrolytes and related labs •

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Diabetes insipidus, cerebral salt wasting or SIADH can occur

Serum glucose, sodium, osmolality

Body position •

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HOB elevated 30-45o (unless cervical injury) •

Facilitates compensation

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Only place HOB flat if you need to maintain CPP

Avoid neck flexion- obstructs venous outflow

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Minimize stimulation when posturing

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Turn client with slow, gentle movements

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Continuous lateral rotational therapy

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Avoid extreme hip flexion (increases intraabdominal pressure and ICP)

Avoid Valsalva maneuver, coughing, straining

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Implement measures to prevent hazards of immobility – rotating mattress or bed, etc.

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Protect from injury (confusion, agitation, seizures)

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Use restraints where needed

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Sedation- as light as possible

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Padded side rails

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Non-stimulating environment

Provide psychological support

7. What are epidural hematomas and subdural hematomas and the clinical manifestations of them? How are they treated? Epidural hematoma (EDH) – blood in the epidural space Subdural hematoma (SDH) – blood in the subdural space Epidural hematoma •

Neurological emergency

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Venous or arterial (middle meningeal artery)

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More common in children/young adults

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Unconsciousness – lucid – deterioration

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Headache, n/v, focal signs

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Needs surgical evacuation to prevent herniation, ICP management

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Associated with head injury

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Lens shaped

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Bleeding from middle meningeal artery

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Develops fast (arterial)

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Fracture across medial meningeal artery groove

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Tx. Surgical evacuation (craniotomy)

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Good prognosis if treated early

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Lethal within hours without intervention

Subdural Hematomas •

Associated with head injury

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Bleeding from bridging vein

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Develop anywhere from •

Less than 72 hrs (acute); 24-48 hrs

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3 to 7 days (sub-acute), or

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weeks (chronic) after injury

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High mortality rate

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Acute, subacute, chronic subdural hematomas

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Acute: (24-48 hrs)

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Decreased LOC

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Increased ICP

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Headaches, ipsilateral pupil fixed if ICP elevated, cerebral edema,

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Cerebral edema increase morbidity & mortality

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SILENT KILLER

Subacute: (2-14 days) •

Enlarge over time as consequence of fluid drawn to subdural space from hematoma breakdown

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MUST BE CAUTIOUS OF BLOOD THINNERS

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Chronic: (weeks-months) •

Common in older adults (brain atrophy increase space)

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Chronic alcoholics

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Focal symptoms more than increased ICP

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Somnolence, confusion, lethargy, memory loss, (can be misinterpreted for stroke, depression, dementia, TIA)

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History of fall or any minor injury

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Causes: Aneurysm vs. AVM (Arteriovenous malformation)

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Secondary damage from rebleeding and vasospasm cause most of the morbidity & mortality

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Clinical presentation: •

Kernig’s sign:

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Brudzinski’s sign:

Meningism

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Low back or leg pain

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Increased temperature, HR, BP,

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EKG changes

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Pituitary dysfunction (DI, SIADH)

8. What are nursing considerations post cranial surgery? Postoperative a. Maintain patent airway b. Prevent/monitor for increased ICP (maximum edema occurs within 24-48 hrs after surgery) c. Monitor vital and neurological signs d. Manage pain, nausea e. HOB at 30 degrees with head in neutral alignment 

Incision management

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Administer medications •

9.     

Corticosteroids – controls cerebral edema •

Dexamethasone

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May be given after craniotomy to reduce edema

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Osmotic diuretics

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Analgesics

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Anti-epileptic drugs

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Anti-emetics

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Antipyretics

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Antibiotics

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Hormonal replacement as needed depending if they have DI or SAIDH

What is bacterial meningitis and the clinical manifestations of it? The most serious form of meningitis About 4,100 cases in the United States every year Common causative agents Streptococcus pneumoniae (Gram +)- older adults Neisseria meningitidis (Gram -)-adolescents & young adults

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Haemophilus influenzae (Gram -) Listeria monocytogenes Group B Streptococcus

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Subjective: •

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Photophobia, nausea, neck and back pain

Objective: •

Severe headache

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Nuchal rigidity

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Fever

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Vomiting

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Focal deficits, signs of increased ICP

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Petechial rash with meningococcus

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Systemic findings

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Most common complication is increased ICP

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Medical emergency

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Antibiotic therapy started after collection of specimens for cultures

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Dexamethasone (corticosteroid) prescribed with first antibiotic dose

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Codeine for pain (no sedation)

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Treat fever to prevent seizures

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Hydration

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Subdural empyema-bacterial meningitis

Spinal tap CSF10.      

What is GCS and what do their values represent? (Is it better to have a high or low GCS)? Ability to speak Obey commands Open eyes to verbal or painful stimulus Gold standard to assess LOC Score range from 3-15; lower the score, higher severity of injury and lower level of brain functioning GCS of 8: coma

11. What is the clinical manifestations and complications of intracerebral hemorrhage? Caused by HTN Increased ICP 12. What are the risk factors for reducing risk of CVA? Why is blood pressure control so important? 27 year old with high blood pressure = risk for CVA 87 year old with high blood pressure for 40 years = immediate risk for CVA Stroke

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Abrupt or rapid onset of a neurological deficit resulting from the interference of blood supply to the brain

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One stroke occurs every 40 seconds, one stroke is fatal every 4 minutes

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30-50% survivors are left with moderate to severe disabilities

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Ischemic or hemorrhagic

Risk Factors •

Nonmodifiable •

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Gender, age (older adults) , race, heredity

Potentially modifiable •

Hypertension, cardiac disease, DM, blood lipid abnormalities, lifestyle habits such as smoking, obesity, alcohol use, diet

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Less than 1 hr

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Transient, focal, may not leave sequelae,

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Medical emergency ischemic event without infarction

TIA

When blood flow to brain is interrupted •

Neuronal metabolism altered within 30 seconds

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Metabolism ceases in 2 minutes

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Cellular death occurs in 5 minutes

Treatment focuses on maintaining blood flow to area surrounding the infarct (ischemic penumbra)

Ischemic Stroke •

80% of strokes

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Extent depends on rapidity of onset, size of damage area, & presence of collateral circulation

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No LOC decrease in first 24hr, progress in 72 hr as infarction & edema develops

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Partial or incomplete arterial occlusion •

Thrombotic –preceded by TIA 30-50%, develop slowly, males (in the brain)

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Embolic – sudden, severe symptoms, recurrent, females (traveled to brain)

Hemorrhagic Stroke •

Bleeding into the brain tissue

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Intracerebral hemorrhage - Poor prognosis – up to 80% mortality in the first 30 days… hypertension biggest cause

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Subarachnoid hemorrhage (ruptured aneurysm) – 40 % of these cases die during the initial bleed/rupture

Clinical Manifestations •

Common findings •

Motor deficits: akinesia, hypo or hyperreflexia

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Communication problems: •

Aphasia: loss of comprehension or produce language

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Dysphasia: ability to communicate

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Dysarthria: pronunciation, articulation, phonation

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Changes in affect and intellectual function

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Spatial-perceptual alterations

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Changes in elimination

Right-sided:  Left hemiplegia  Left neglect  Spatial-perceptual deficits  Denial  Short attention span  Impulsive  Impaired judgment  Impaired time sense Left-sided:  Right hemiplegia  Impaired language  Impaired...