Central Nervous System and Increased ICP Flashcards

1
Q

Identify the structural components of Central Nervous System (CNS) and the function of each

A

Brain stem
Midbrain
Pons
Medulla
-vital centres concerned with respiratory,
vasomotor, and cardiac function are
located in medulla
——————————————————————————

Cerebellum
-Coordinates voluntary movement & maintains
trunk stability, and equilibrium

Cerebrum: left and right cerebral hemispheres. Important for care. Lobes have functions

Frontal Lobe
-Controls higher cognitive functions, memory, voluntary movements,
-Broca’s area in (L) hemisphere (for expressive speech & language

Temporal
-Wernicke’s area (responsible for receptive language)
-Integration of somatic, visual, and auditory data

Parietal
-Composed of sensory cortex
-Controls and interprets spatial formation

Occipital
-Processes visual data

Ventricles:
-4 cavities within the brain, filled with CSF
——————————————————————————

Spinal cord
Ascending tracts
Descending tracts
Lower motor neurons
Upper motor neurons
Reflex arc

Cerebro-spinal fluid:

-Clear, colorless, Carries nutrients
-Circulates within subarachnoid space
-Provides cushioning for brain and spinal cord
-Allows fluid shifts from cranial cavity to spinal cavity
-Fluid moves depending on the pressure from
cranial to spinal cavity
-Absorbed through arachnoid villi
-CSF pressure is measured in pts with actual or suspected intracranial diseases
-increase in CSF pressure indicates- intracranial pressure (ICP) _ can lead to herniation of brain
-Brain herniation: pushing brain in area its not
supposed to be in. Bleeding in brain, tumor
grows = pushs pressure -> too much pressure
prolonged = cerebral ischemia and death to the
cells

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2
Q

Cerebral circulation & protective structures

A

Blood-Brain Barrier:

-Physiological barrier between blood capillaries and brain tissue

-Protects brain from certain harmful agents, while allowing nutrients

-Affects penetration of drugs → only certain ones enter
-Lipid-soluble drugs enter quickly
-Water-soluble and ionized drugs enter slowly

Protective structures of brain:
-Meninges
-Meninges are 3 layers of protective membranes that surround brain and spinal cord:
1. Dura matter- Outermost layer
2. Arachnoid- Delicate, impermeable membrane. Arteries, veins, and cranial nerves passing to and from brain must mass through subarachnoid space
3. Pia matter -Delicate, innermost layer of meninges

-Skull
-Vertebral column

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3
Q

Explain the mechanisms that regulate normal intracranial pressure (ICP).

A

A closed space what does this mean for rising pressure? -pressure has nowhere to go

vol from 3 components: _Cerebrospinal fluid, blood, brain tissue are in the brain

Monroe Kelly hypothesis- If vol of any of 3 components ↑ without corresponding ↓ in another component → results in ↑ ICP

Measure of ICP
In ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer

Normal ICP: 5- 15 mmHg
Sustained ICP >20 mmHg = abnormal

Compensatory mechanisms:

-Mechanisms to resist ↑ in ICP by:
1) Changes in CSF volume
-by displacement of CSF, e.g., into spinal subarachnoid space
or
-altering production and absorption rates of CSF

2) Altering intracranial blood volume
-by compression of veins, or vasoconstriction/vasodilation, or changes in venous outflow

3) Brain tissue volume compression
-Distention of dura, or compression of brain tissue

*However, compensatory adaptations are finite

Brain has ability to autoregulate its own blood flow in response to metabolic needs (= called autoregulation
-Autoregulation does not work in extreme hypo/hypertension

Automatic alteration in diameter of cerebral flow to maintain constant blood flow

Brain is unable to store oxygen and glucose=Always have to have a supply of blood flow to get glucose and O2
-MAP should be 65 mmHg
-if MAP <50 =Cerebral Blood Flow decreases, cerebral ischemia occurs
-if MAP > 150 mmHg, cerebral vessels are maximally constricted, and further response is lost

Other factors affecting CBF:

↑ PaCO2 <50 mmHg → vascular dilation, increasing CBF.
=increases blood flow to brain
- causes cerebral vasodilation, ↓ vascular resistance, and ↑ cerebral blood flow (CBF)
-In acidotic environment, further vasodilation in attempt to ↑ blood flow
-if carbon dioxide is decreased in the blood this is reversed and CBF is decreased.

CBF can be indirectly reflected by calculating cerebral perfusion pressure (CPP)
-CPP is the pressure needed to ensure adequate perfusion to brain tissue

  -MAP minus ICP = CPP
  -CPP is 70-100  (normal)
  -CPP 50-60  (adequate)
  -CPP <50 (cerebral ischemia)
  -Less than 30 (not capatible with life)

*CPP does not reflect perfusion pressure in ALL parts of the brain

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4
Q

Describe the common etiologies of increased intracranial pressure

A

Secondary injury resulting from hypoxia, ischemia, hypotension, edema, increased ICP that follows a primary injury several hours-days after the 1st injury

ICP causes cerebral ischemia and death

causes of ↑ ICP:

Cerebral edema
- ↑ accumulation of fluid in extravascular
spaces of brain tissue
-Different types:
Vasogenic cerebral edema
Cytotoxic cerebral edema
Interstitial cerebral edema

Contusion
-bruise. Can cause bleeding and swelling

-Cerebral abscess
-puss filled pocket of infected material. Can cause brain to swell, pressure on it, keep blood from flowing to part of the brain. Caused by bacteria that comes in from blood infection, meningitis, encephalitis, sx, ear infection, sinus infection.
-Needs emergency tx

-Cerebral neoplasm

Risks increase: heart effects, HIV/aids, immunosuppression, recent injury/sx to head, tumor, hx IV drug use

cerebral edema types continued:

  1. Vasogenic cerebral edema
    -Most common type
    -From changes in endothelial lining of cerebral capillaries
    -↑ in permeability of blood-brain barrier and ↑ extracellular fluid vol
    -Occurs mainly in white matter
  2. Cytotoxic edema
    -From disruption of integrity of cell membrane
    -Results from destructive lesions or trauma to brain tissue, leading to cerebral hypoxia/anoxia, Na+ depletion, syndrome of inappropriate antidiuretic hormone (SIADH)
    -Fluid and protein shift from extracellular space into cells
    -Most often in grey matter
  3. Interstitial cerebral edema
    -Result of diffusion of ventricular CSF in an uncontrolled hydrocephalus, leaks into surrounding tissues
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5
Q

clinical manifestations of increased intracranial pressure at the early, late and terminal stages.

EARLY

A

First indicator: change in LOC. Confusion, flat affect (face and voice on one level), level of attention (just seem off)

  EARLY SIGNS Altered LOC: -Vomiting, headache, seizures -Unilateral pupil changes in size, equality, and/or reactivity -papilledema - swelling of the optic nerve = eyes bulging out of sockets -Altered respiratory pattern, e.g., bradypnea, or irregular -Unilateral hemiparesis
      -Focal finding – in area of lobes

Weakness to one side of the body

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6
Q

LATE SIGNS

A

↓ LOC (stupor)
-Unilateral or bilateral pupillary changes, i.e. size,
equality, and/or reactivity
-Cheyne-Stokes respiration - alterations of fast shallow, stop, and deep resps
-Decorticate or decerebrate posturing
(deCORticate - arms flexed towards core)
(decerebrate) - arms flexed outwards WORSE

Cushing’s triad:
-bradycardia (slow HR)
-irregular resps (slower)
-widening pulse pressure (increased SBP)

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7
Q

TERMINAL

A

TERMINAL

Coma

Bilaterally fixed and dilated pupils

Resp. Arrest
-dt ↑ ICP with compression of brain stem and respiratory centre = increase PaCO2 = vasodilate = more blood flow to brain

Absence of motor response

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8
Q

Causes of cerebral edema

A

Mass lesions:

-Brain abscess
-brain tumor
-Hematoma
-hemorrhage

Head injuries:

-Contusion
-Diffuse axonal injury
-Hemorrhage
-Post-traumatic brain swelling

Cerebral infections:

-Meningitis
-Encephalitis

Brain surgery

Vascular insult:

-Anoxic & ischemic episodes
-Cerebral infarction (thrombotic or embolic)
-Venous sinus thrombosis
(-clot forms in sinuses and prevents blood from draining = hemorrhage)

Toxic or metabolic encephalopathic conditions:

-Hepatic encephalopathy
-Lead or arsenic intoxication
-Uremia
-causes kidney fail – toxins build up

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9
Q

Complications

A

Inadequate cerebral perfusion

Cerebral herniation:

(Brain tissue forcibly shifts from greater pressure to lower pressure area).

Pressure on brain stem = likely to die

-Cingulate herniation (most common)
(midline shift (don’t want a midline shift) -brain tissue pushed across midline. Damage on one side/bleeding and edema on other side

-Tentorial herniation
-Cerebellar tonsillar herniation
-moves downwards to base of skull where
spine connects to brain

-Falx cerebri
-Tentorium cerebelli
-Tentorial incisura
-one that goes downwards near brain stem, inparticular the medulla

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10
Q

Interprofessional Care

A

Interprofessional Care:

Drug therapy:
-Mannitol -osmotic diuretic. Fluid moves from brain to blood vessels , excreted by kidneys
-Hypertonic saline -has lots of Na (3%), reduced edema because draws water out into veins
-Corticosteroids -reduce swelling, inflammation
——————————————————————————
Pain control!!!

*Pain control would cause sedation = affect GSC – so they don’t give pain med while checking GSC q1h

Nutritional therapy:
-Hyper metabolic and hyper catabolic state- increase need for glucose and O2

Supportive therapy:
-Metabolic demands such as fever, agitation, shivering, pain, and seizures can ↑ICP

-Induced coma!!!!
-given a barbiturate. -for 3 days why – brain is always active but in an injury, don’t want an active brain because only healing is when the brain is resting and sleeping. Breathing tube.

-Inducing hypothermia to suppress cerebral metabolism. This is done often for several days but extended hypothermia makes the patient suspeptible to systemic infections and hypotension

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11
Q

Diagnostic studies

A

MRI
CT scan
MRA (magnetic resonance angiography)
CTA (computed tomographic angiography)
Above tests are used to differentiate many conditions that can cause _ ICP and to evaluate therapeutic options

Top three: evaluate ICP, see if getting better

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12
Q

Describe the nursing care of the patient with increased intracranial pressure.

A

Glasgow coma scale

eye-opening /4
verbal response /5
motor response /6

minor brain injury 13-15
moderate brain injury 9-12
severe brain injury 3-8

*Score less than or equal to 8 at 6 hours post injury - 50% die

Neurological assessment:
-VS
-Pupils compared for size, movement, and response (use penlight).
-Evaluate cranial nerves.
-For unconscious patients, observe their spontaneous movement.
-If no spontaneous movement, painful stimuli are applied.

one pupil dilated = compressed cranial nerve III
bilateral dilated + fixed = OMINOUS SIGN
pinpoint = drugs or pons damage

Respiratory function:

-airway- intubating during coma
-Body position- do not lie flat. Elevated at least 30 degrees to promote venous drainage from head. ———Turn slowly. Keep head midline, not to the side

Fluid & electrolyte balance
——————————————————————————
Monitoring ICP
——————————————————————————
Protection from injury- confusion, agitation, seizures:
-always risk of seizure with brain trauma = anti-seizure medication and seizure precautions, restrained if confused
-Barbituate induced coma
-Coughing, straining and Valsalva manoeuver =avoid

*Any stimulation =avoid

Psychological consideration

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