Neuro Part 1 Flashcards

1
Q

Levels of Consciousness

A

Alert
Confused
Lethargic
Obtunded: Arousable with stimulation, but sleepy. Follows simple commands
Stuporous: Very hard to arouse
Semicomatose: Purposeful movements
Comatose: Reflexive responses, no verbal responses

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2
Q

Decreased LOC: Nursing care

A
Avoid narcotics for pain to determine declining neuro status
Airway
Vital signs
Neuro checks
Protect eyes
Nutrition
Prevent skin breakdown
Safety (Fall risk)
Psychosocial
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3
Q

Oculocephalic reflex-Doll’s Eyes

A

Rotate patient’s head to one side and observe movement of eyes.
(NEVER do this if a C-spine injury is suspected)

Normal response—initial conjugate deviation of the eyes in the OPPOSITE DIRECTION, then in a few seconds, both eyes move back to midline.

Normal response indicates an intact brainstem.

Doll’s Eyes present: positive, a good thing, brainstem is intact

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4
Q

Oculovestibular reflex-caloric ice water test

A

Elevate head 30 degrees

Instill 30-50 mls iced water into ear (one at a time)

Patient MUST have intact eardrum and no skull fracture

Patient’s eyes should look TOWARD the irrigated ear
Shows intact midbrain and pons

*NEVER, EVER perform a lumbar puncture on a patient with elevated ICP or a patient who is coagulopathic!

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5
Q

Lumbar Puncture

A

Keep patient laying supine for 8-10 hours. Flat is best
Well hydrated
Check CSF for glucose, WBC’s, protein, infection, etc.

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6
Q

Increased Intracranial Pressure

A

Monroe-Kellie Hypothesis states that a change in volume of any one component must be accompanied by a reciprocal change in one or both of the other components. If this reciprocal change is not accomplished, the result is an increase in Intra-cranial Pressure (ICP).

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7
Q

Factors that influence ICP changes are:

A
Arterial & venous pressure	
Intra-abdominal and intra-thoracic pressure
Posture
Temperature
Blood gases, particularly CO2 levels
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8
Q

Causes of increase in ICP:

A
Head trauma
Stroke
SAH
Brain tumor
Inflammation
Hydrocephalus
Brain tissue damage due to other causes
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9
Q

Clinical Manifestations of Increased ICP

A

**Changes in LOC: First sign
**
Changes in VS
Sudden change in ICP - Cushing’s triad: Increased pulse pressure, decreased pulse, and changes in respiratory pattern with pupillary changes. Could be herniation of brain tissue.
Motor changes (contralateral)
Pupillary changes / Ocular signs (ipsilateral)
Headache/vomiting
***Respiratory pattern: Early sign (hyperventilate, low C02)

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10
Q

Complications of Increased ICP

A

Tissue ischemia

Tissue compression (herniation)
When the structures of the brain are compressed, hormonal functions are affected:

***Diabetes insipidus (neurogenic) results when there is insufficient ADH released from the pituitary. Fluid and electrolyte imbalances occur. Causes increased urinary output with very low urine specific gravity and urine osmolality. Plasma osmolality is INCREASED due to hypernatremia and dehydration.

***Peeing a lot, replace fluids. Hypovolemic/hypotensive patients need preserved brain tissue, give fluids to compensate

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11
Q

Complications of Increased ICP: SIADH

A

SIADH- results when high ADH production occurs. Pt has fluid retention, low serum osmolality, dilutional hyponatremia, and concentrated urine and increased weight. They are ‘holding on’ to fluid.

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12
Q

Monitoring ICP

A

A catheter is placed into the brain that will give us a waveform and a pressure reading continuously.

Some systems allow CSF to be drained so that the pressure can be lowered.

***Hematoma, low GCS are indications for a ventricular catheter

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13
Q

Intracranial Pressure Monitoring

A

Normal ICP: 0-10, 15 is upper limit normal mm Hg

Sustained pressure >15 = abnormal

ICP HTN > 15 mmHg
Associated with increased risk of secondary brain damage

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14
Q

Locations for monitoring/measuring ICP

A

Subarachnoid Space - waveform is dampened due to the bone and tissue- no CSF drainage

Intraparenchymal- in the brain tissue, OK waveform but no CSF drainage

Intraventricular - gold standard. Excellent waveform and CSF drainage possible. High risk for infection.

Epidural space – Good waveform and CSF drainage is possible.

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15
Q

Managing elevated ICP

A

Mean Arterial Pressure (MAP)=Systolic BP+2(Diastolic BP) divided by 3

Cerebral Perfusion Pressure (CPP)—this tells us how well the brain is being perfused.

Normal CPP =70-80mmHg.
To calculate the CPP: CPP=MAP-ICP

CPP < 60mmHg there is a decrease in blood supply to the brain this will not provide adequate cerebral perfusion and oxygenation. neuronal hypoxia and cell death may occur.

CPP> 100 mmHG there is a potential for Hyperperfusion and increased ICP

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16
Q

Goal of Therapy -Reducing ICP:

A

**CSF drainage-no more than 30cc at a time
**
Decrease edema with osmotic diuretics-Mannitol
**Proper positioning to optimize venous drainage-keep head and neck aligned and HOB elevated at 30 degrees
Preservation of cerebral oxygenation and perfusion
Early identification of neuro changes
Prevention of complications
**
Surgical intervention-partial lobectomy to remove damaged tissue or hemicraniectomy (bone removed until edema resolved).

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17
Q

Pharmacological Management of ICP

A

Mannitol- powerful osmotic diuretic–can be given as intermittent IV boluses depending on the ICP. MUST monitor serum osmolarity, usually q6H (keep < 320mOsm or hypovolemia and renal failure occur).

IV hypertonic saline (1.8%, 3% or 7.5%). Also decreases brain tissue volume. Needs central line and EKG monitoring.

Continuous IV sedation
Possible neuromuscular blockade (NMB)
Possible barbiturate coma if all else fails (Phenobarbital)-decreases cerebral tissue demands
Anticonvulsants (Phenytoin or Fosphenytoin)

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18
Q

Mechanical ventilation for Increased ICP

A

Keep PaCO2 within normal range but the lower end of normal (35-40)

Hypocapnia results in cerebral vasoconstriction, while hypercapnia increases cerebral blood flow and therefore the volume of blood within the skull

Minimize suctioning/coughing/Valsalva-will raise ICP hence need for sedation and/or NMB

19
Q

Brain Temperature Monitoring

A

Brain temperature is generally 0.5-1.0 degree C higher than core body temp

Therapeutic hypothermia is currently being explored in early brain injury recovery to prevent secondary brain injury

20
Q

Increased ICP: Nursing care

A
Diagnostics: CT, MRI
GCS and Neuro Assessments
IV fluids
Regulate temperature
Decrease stimuli (space out activities)
21
Q

Brain Tumors S/S

A

**Headache, worse at night, mental status changes (FIRST SIGN of increased ICP)

Seizures
N&amp;V
Cognitive dysfunction
Motor dysfunction (assess gait)
Increased ICP
22
Q

Brain tumors: treatment

A

Surgery – craniotomy
Tumors may be inoperable because of their location

Radiation

Chemotherapy

23
Q

Cerebral Ischemia

A

The ischemic cascade begins within seconds to minutes after perfusion failure, creating a zone of irreversible infarction and a surrounding area of potentially salvageable “ischemic penumbra.” The goal of acute stroke management is to salvage the ischemic penumbra

24
Q

Hemorrhagic stroke

A

Hypertension often is a precipitating factor. Vascular abnormalities, such as AVMs and cerebral aneurysms, are more prone to rupture and cause hemorrhage in the presence of hypertension.

25
Q

Diagnosis for Stroke

A

Rapid diagnosis of a stroke is essential so that appropriate patients can receive thrombolytic therapy, the goal of which is to save damaged brain tissue and minimize permanent deficits.

3-hour window for thrombolytic therapy

Pt with S & S of stroke needs immediate CT head without contrast to r/o bleeding

If no bleeding, stroke assumed to be thrombotic—pt may be candidate for TPA (lots of exclusion criteria)

26
Q

Ischemic or Embolic Stroke treatments

A

Thrombolytic therapy within 4.5 hours of symptom onset.
Anticoagulant / antiplatelet therapy

Management of increased ICP and cerebral edema
BP management

Strict glycemic control (poor outcomes associated with hyperglycemia—increases cerebral edema)

Fever control / induced hypothermia (still being researched but becoming more common)

27
Q

Thrombolytics

A

Thrombolytic therapy should be initiated within 4.5 hours or less of the onset of neurological symptoms. The clock begins for the patient from the time he or she was last seen well.

*Intraarterial TPA has a window of 6 hrs

28
Q

Thrombolytics: TPA

A

TPA is usually given IV over an hour.

Can also be given intra-arterially (requires specialist monitoring and care). Introducer placed in femoral artery, catheter advanced into carotid artery for TPA administration.

***Can be effective up to 6 hours after onset of symptoms BUT major risk of bleeding.

29
Q

Hemorrhagic Stroke

A

Intracranial hemorrhage is bleeding directly into the brain matter

Usually occurs at the bifurcations of major arteries at the base of the brain (usually due to a rupture of an aneurysm or AVM)

Can result from HTN, anticoagulants, amphetamines, illicit drugs, brain tumors eroding vessels

30
Q

Symptoms of Hemorrhagic Stroke

A

Similar to ischemic stroke (numbness, weakness, hemiparesis, confusion, dizziness, difficulty speaking)

but also:
Sudden severe headache (“worst headache of my life”)
Vomiting more common
Seizures more common
Nuchal rigidity (from meningeal irritation)
Visual disturbances

31
Q

Cerebral Edema

A

Vasogenic Edema—after the injury, influx of fluids and solutes enter the brain through an incompetent blood-brain barrier. More common

Cytotoxic Edema—cellular swelling that occurs in brain ischemia and trauma.

Edema can lead to increased ICP, tissue shifts, brain displacement

32
Q

Subarachnoid Hemorrhage (SAH)

A

Bleeding surrounding the brain tissue in the subarachnoid space.

Common causes: AteriouVenous Malformation, cerebral aneurysm (usually at the circle of Willis), HTN, trauma.

33
Q

Subarachnoid Hemorrhage (SAH) con.t.d

A

Symptoms: sudden, severe headache, vomiting, seizures, meningeal irritation

Dx: CT, LP

Medical treatment: ***avoid vasospasm
- Calcium channel blocker – Nimodipine, Nicardipine - Volume expansion

34
Q

SAH complications

A

Cerebral vasospasm is a serious complication of SAH

Medications such as Nimodipine (Nimotap) or Nicardipine (Cardene) can help prevent cerebral vasospasm.

35
Q

Hemorrhagic StrokeTreatments

A

BP control (not too high, not too low)

Aneurysm precautions (quiet environment, stool softeners to prevent straining, limiting visitors)

Elevation of HOB to 30 degrees
Pain control for headache
Surgical repair if possible
Prevention of vasospasm

***Be aware: Many patients survive the initial bleed then rebleed 24-48 hours later. It is usually fatal at this point.

36
Q

Nursing Considerations for Stroke

A

DVT prophylaxis

Neurological: Monitor for changes in status, Glasgow Coma Scale, seizures

Musculoskeletal: elevate weak side, proper body alignment

Integumentary: Q2H position changes, special mattresses

GI: Speech therapy

37
Q

Nursing Considerations -Communications

A

Left hemisphere dominant for language
Aphasia – total loss of comprehension and use of language

Dysphasia – partial loss of communication
Receptive: Not understanding your speech/ (Wernicke’s area)

Expressive: Frontal lobe damage, can’t vocalize
(Broca’s area)

Dysarthria – motor control of speech, low articulation

38
Q

Nursing Considerations for brain injuries

A

Right brain injury- poor judgment, spatial-perception deficits, impulsive

Left brain injury- cautious, language deficits, high frustration

Homonymous hemianopsia (blindness in the same half of each visual field) is common after a stroke. Persistent disregard of objects placed in one area of the visual field should indicate to the nurse that this is present

39
Q

AVM’s

A

In AVMs, high flow arterial blood shunts directly into low resistance venous vessels

Intravascular pressure is increased
Leads to potential ruptures

40
Q

AVM Presentation and Diagnosis

A

Presentation
Intracerebral hemorrhage (38-70%)
Parenchymal, subarachnoid, intraventricular, or a combination
Seizure activity
Headache
Focal neurological deficits sometimes seen

Diagnosis
CT of head
With / without contrast
MRI
4 vessel angiography
41
Q

AVM Treatment

A

Endovascular embolization: inject substances to occlude a vessel

42
Q

Cerebral Aneurysm Presentation

A

Unruptured
Asymptomatic in many cases
May have: headache, palsies, extraoccular motor deficits, vision changes, pain above or behind the eye, nuchal rigidity, seizures, photophobia

Ruptured
Cranial hemorrhage
Severe headache, nausea, vomiting, cranial nerve deficits, stiff neck, blurred vision, seizures, HTN, bradycardia, localized motor weakness

43
Q

Cerebral Aneurysm Treatment

A

Measures of aneurysm size before and after

Surgical clipping or repair required
Coiling or stent

Pre-surgery focus is on BP control and symptom management

44
Q

Cerebral Aneurysm Nursing Care

A

Prevent re-bleeding: “aneurysm precautions”
Quiet environment, bowel regimen, limiting visitors
Pain management
Antipyretics and cooling blanket for fevers
Manage increased ICP
Monitor for vasospasms