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Critical Care Exam 4 > TBI > Flashcards

TBI Flashcards

1
Q

s/s of intracranial hypertension (increased intracrainial pressure-ICP

A

Cushing triad, diminished brainstem reflexes, papilledema, decerebrate posturing (abnormal externsion), decorticate posturing (abnormal flexion) unequal pupil size, projectile vomiting, decreased pupillary reaction to light, altered breathing patterns, and headache.

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2
Q

Early signs of ICP

A
  • Decreased level of consciousness
  • Papillary dysfunction
  • Motor weakness
  • Sensory deficits
  • Cranial nerve palsies, dysfunction of extraocular eye movements (EOM)
  • Headache
  • Seizures
  • The earliest, most sensitive sign is the change in level of consciousness
  • Watch for localized neurological symptoms
  • Slowing of speech
  • Delay in response to verbal stimuli
  • Restlessness
  • Confusion
  • Increased drowsiness
  • pupillary dysfunction
  • motor weakness/sensory deficits
  • H/A, Seizures
  • cranial nerve palsies
  • dysfunction of extraocular eye movements (EOM)
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3
Q

Late signs of ICP

A 
Late Signs and Symptoms of ICP
•	Continued deterioration in LOC (coma)
•	Vomitting
•	Papiledema
•	Headache
•	Hemiplegia, Decortication, or decerbration
•	Cushing triad
•	Impaired brain stem reflexes
  • pupillary changes
  • Cushing’s triad (increased systolic blood pressure (SBP), widened pulse pressure, and bradycardia)
  • Continued deterioration in LOC (coma)
  • Vomiting
  • H/A
  • papilledema (swelling of the optic disc)
  • hemiplegia
  • decortication, or decerebration (worse)
  • impaired brain stem reflexes (lack of pupillary, corneal, gag, swallowing, doll’s eyes)
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4
Q

Cushing’s Triad

A

increased systolic blood pressure (SBP) widened pulse pressure, and bradycardia

(bradycardia, hypertension, and bradypnea)

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5
Q

Normal Value ICP

A

mean ICP is kept below 15 mm Hg

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6
Q

Medical Interventions ICP

A
  • Cerebral perfusion pressure (CPP)
  • Cerebrospinal fluid drainage
  • Hypnotics/sedatives
  • Osmotic diuresis (mannitol) –
  • Carbon dioxide control (PaCO2 35-45)
  • Temperature control (antipyretics)
  • Barbiturates (phenobarbital and pentobarbital - barbiturate coma)
  • Paralytics
  • Lidocaine before suctioning
  • Hypertonic saline
  • Anticonvulsant (phenytoin; dilantin and fosphenytoin; cerebyx) – Neuromuscular Blocking agents
  • Surgery
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7
Q

Nursing Interventions ICP

A
  • HOB should be elevated 30-45 degrees
  • Maintain head alignment
  • Provide good pulmonary toiletry
  • Space nursing care activities to prevent overstimulation
  • Use caution when suctioning patient
  • Use hyperventilation with 100% oxygen before suctioning
  • Maintain blood pressure in high normal range for patient
  • Space nursing activities
  • Avoid bright lights and noise
  • Speak softly
  • Use gentle touch
  • Encourage family contact
  • Monitor for seizure activity
  • Pad hard surfaces
  • Avoid: Trendelenburg, prone, extreme flexion of the hips, angulation of the neck, PEEP > 20 cm H2O, coughing, suctioning, tight tracheostomy tube ties, Valsalva maneuver
  • Repetitive neurologic assessments - GCS, maintain airway, maintain head alignment, maintain normothermia below 100.4 (cooling blanket)
  • control ventilation to ensure PaCO2 35 – 45
  • ensure CPP > 70mmHg
  • drain CSF for ICP > 20 mmHg
  • reduce environmental stimulation
  • seizure control
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8
Q

Nursing Interventions ICP

A
  • HOB should be elevated 30-45 degrees
  • Maintain head alignment
  • Provide good pulmonary toiletry
  • Space nursing care activities to prevent overstimulation
  • Use caution when suctioning patient
  • Use hyperventilation with 100% oxygen before suctioning
  • Maintain blood pressure in high normal range for patient
  • Space nursing activities
  • Avoid bright lights and noise
  • Speak softly
  • Use gentle touch
  • Encourage family contact
  • Monitor for seizure activity
  • Pad hard surfaces
  • Avoid: Trendelenburg, prone, extreme flexion of the hips, angulation of the neck, PEEP > 20 cm H2O, coughing, suctioning, tight tracheostomy tube ties, Valsalva maneuver
  • Repetitive neurologic assessments - GCS, maintain airway, maintain head alignment, maintain normothermia below 100.4 (cooling blanket)
  • control ventilation to ensure PaCO2 35 – 45
  • ensure CPP > 70mmHg
  • drain CSF for ICP > 20 mmHg
  • reduce environmental stimulation
  • seizure control
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9
Q

Management of Increased ICP: CPP

A
  • Less aggressive at treating hypertension to enhance CPP
  • Avoid hypotension
  • Goal: Maintain MAP greater or equal to 80 and CPP greater or equal to 60
  • May use vasopressors to increase MAP:
  • Phenylephrine (Neo-Synephrine)
  • Dopamine (Intropin)
  • Norepinephrine (Levophed)
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10
Q

Management of Increased ICP: Cerebral Fluid Drainage

A
  • Treatment of increased ICP includes drainage of CSF
  • Drain via intraventricular catheter (IVC) connected to an external ventricular draining (EVD) system
  • May be performed intermittently or continuously
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11
Q

Management of Increased ICP: Hypnotics/Sedatives

A
  • Can be used to decrease ICP and lower cerebral metabolism
  • Opioids and benzodiazepines help manage pain and agitation
  • Propofol (Diprivan) is a sedative used for its short-acting effect
  • Very careful with amount give, can completely knock out respirations, weight based, never give more than 50 miks/kilo/min – propofol infusion syndrom
  • Bispectral (BIS) index monitor may be used to assess degree of sedation
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12
Q

Management of Increased ICP: Osmotic Diuretics

A
  • Increases intravascular osmolality
  • Draws fluid from the brain tissue, lowering cerebral edema and ICP
  • Montior serum osmolatiy levels (do not admin if >320 mOsm/L)
  • Hold if Na >151
  • Causes diuresis and volume depletion
  • Replace fluid losses with crystalloids or colloids
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13
Q

Management of Increased ICP: Hyperventilation Issues, CO2 control

A
  • Hyperventilation can decrease ICP by causing cerebral vasoconstriction
  • Cerebral vasoconstriction decreases CBF
  • Maintain normal PaCO2 (greater than or equal to 35 mmHg)
  • Avoid hypercarbia (PaCO2 > 45 mmHg)
  • Chronic, prohplyactic hyperventilation (
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14
Q

Management of Increased ICP: Temperature Control

A
  • Fever increases metabolic rate by 4-14% per degree C
  • Fever increases metabolism/oxygen consumption
  • Even moderate hyperthermia worsens outcomes
  • Early induced mild/moderate hypothermia not recommended in guidelines
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15
Q

Management of Increased ICP: Barbiturate Coma

A
  • Sedative/hypnotic agent
  • Administer as a continuous infusion to protect brain from ischemia
  • Decreases cerebral metabolic rate
  • Monitor burst suppression with EEG
  • Considered a “second-tier” therapy
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16
Q

Management of Increased ICP: Neuromuscular Blocking Agents

A
  • NMB agents cause complete paralysis of all skeletal muscles
  • NMBs are not routinely used for brain-inured pts
  • NMB usage requires mechanical ventilation
  • NMB agent is not a sedative or analgesic!
  • Patient will require sedation
  • Use train of four (TOF) twitch monitoring)
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17
Q

Steroids and ICP

A
  • Have never been found to be effective in improving outcomes for severe TBIs
  • Increase complication risks, such as hyperglycemia
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18
Q

Hyperglycemia and ICP

A
  • Hyperglycemia has been found to worsen neurological outcomes
  • Exacerbates ischemic acidosis
  • Frequent glucose monitoring for serum glucose control
  • Avoid IV fluids with dextrose because it may cause hyperglycemia and cerebral edema
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19
Q

Hyperglycemia and ICP

A
  • Hyperglycemia has been found to worsen neurological outcomes
  • Exacerbates ischemic acidosis
  • Frequent glucose monitoring for serum glucose control
  • Avoid IV fluids with dextrose because it may cause hyperglycemia and cerebral edema
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20
Q

Management of Increased ICP: Surgical

A
  • Crainotomy: opening of the cranium to remove, at minimum, a blood clot or mass lesion
  • Craniectomy: the piece of bone removed during the craniotomy is not replaced at the end of surgery
  • Allow to swell outside skull then replace skull
  • Skull is put in abdomen
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21
Q

concept of Monroe-Kellie hypothesis

A

When one intracranial component increases in volume, the others have to decrease in volume so that there’s an equal total volume. This includes: displacing CSF from the intracranial vault to the lumbar cistern, increasing CSF absorption, and compressing the low-pressure venous system

involves brain substance, CSF, and blood

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22
Q

what is herniation?

A

Herniation of intracerebral contents results in the shifting of tissue from one compartment of the brain to another and places pressure on cerebral vessels and vital function centers of the brain. Unchecked can rapidly cause death.

Classic sign of herniation is increased BP to help oxygenate brain tissue, short run of tachy before brady

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23
Q

Uncal herniation:

A

Most common herniation syndrome
Unilateral herniation expanding mass lesion, usually of the temporal lobe, increases ICP causing lateral displacement of the tip of the temporal lob (uncus). Lateral displacement pushes the uncus over the edge of the tentorium, puts pressure on the oculomotor nerve (cranial nerve III) and the posterior crerebral artery ipsilaterl to the lesion, and flattens the midbrain against the opposite side.

24
Q

s/s of uncal herniation:

A

Ipsilateral pupil dilation, decreased LOC, respiratory pattern changes leading to respiratory arrest, and contralateral hemiplegia leading to abnormal flexion (decorticate), or abnormal extension (decerbrate) posturing.

If no interventions done, then fixed/dilated pupils, flaccidity, and respiratory arrest! Blown dilated pupil-significant for uncal herniation!!!!

25
Q

If patient exhibited s/s of uncal herniation, what would you do?

A

Call the physician, call for help, stay with patient, maintain airway, and assure IV access.

26
Q

What is positive doll’s eyes?

A

Oculocephalic reflex, the eyes deviate to the opposite direction in which the head is turned

27
Q

Absent doll’s eyes?

A

The eyes remain midline with the direction the head is turned

28
Q

What is an intraventricular catheter?

A

A catheter placed into the ventricles via burr hole

It is a catheter that is used to help drain cerebralspinal fluid which in turn will help manage increased ICP. The catheter is conncected to an external ventricular draining system.

29
Q

What is an intraventricular catheter purpose?

A

For ICP monitoring, drainage of CSF, access for contrast media instillation

30
Q

What is cerebral perfusion pressure (CPP)?

A

Blood pressure gradient across the brain

31
Q

How is CPP calculated?

A

calculated as the difference between the incoming mean arterial pressure and the opposing ICP on the arteries. (CPP=MAP-ICP)

32
Q

What is normal cerebral perfusion pressure?

A

50-70 mm Hg

With a patient who has a traumatic brain injury, you want the CPP to be 60-70.

33
Q

What is the relationship between CPP and ICP?

A

A rise in ICP will increase CPP, if there is a decrease in ICP, CPP will decrease. MAP must be adjusted to maintain CPP. (ICP 0-15) (CPP >60)

34
Q

What is MOA of Mannitol?

A

It increases urine flow by creating an osmotic force within the lumen of the nephron. Most of the drug remains in the nephron creating an osmotic force that inhibits passive reabsorption of water. The degree of diuresis is related to the amount of mannitol in the filtrate.

Osmotic Diuretic - MOA – increases intravascular osmolality, draws fluid from the brain tissue, lowering cerebral edema and ICP, causes diuresis and volume depletion decreasing CVP.
Causes vasospasm, increases cerebral blood flow and induces cerebral vasoconstriction to keep blood flow constant reducing increased ICP

35
Q

What role do barbiturates play in the head injury patient?

A

(pentobarbital and thiopental)
For the management of uncontrolled ICP that has not responded other tx. To reduce ICP to 15-20 mm Hg and mean arterial pressure of 70-80 mm Hg. Decrease metabolic rate and oxygen consumption to affect cardiac output.
sedative/hypnotic agent (pentabarbital), administered as a continuous infusion to protect brain from ischemia, decreases cerebral metabolic rate, monitor burst suppression with EEG, considered a “second tier” therapy.

36
Q

What role do osmotic diurectics play in the head injury patient?

A

increases intravascular osmolality, draws fluid from the brain tissue, lowering cerebral edema and ICP, monitor serum osmolality levels (if >320 don’t give, normal is 280-290), causes a diuresis and volume depletion, replace fluid losses with crystalloids or colloids, sodium > 151 hold the drug.

(mannitol) Treats cerebral edema by pulling fluid from the extravascular space into the intravascular space; requires intact blood-brain barrier. Increases intravascular osmolality, draws fluid from the brain tissue placing it into general circulation, increases circulating blood volume increasing workload of the heart, lowering cerebral edema and

37
Q

What role do loop diuretics play in the head injury patient?

A

they help pull of fluids and keep brain edema down as well.

(bumex) – enhance diuresis to remove excess circulating volume decreasing workload on the heart

38
Q

What role does “hyperventilation” play in controlling ICP?

A

Hyperventilation can lead to reduced cerebral perfusion. If you lower PaCo2 to 25-30 then vasoconstriction of the cerebral arteries can occur, reduction of CBF, and increased venous return will result.

39
Q

What PaCO2 level should be maintained in the patient prone to increased ICP?

A

25-30 mmHg

40
Q

Epidural hematoma –

A
  • Arterial bleed
  • Rapid onset of symptoms
  • Risk of uncal hemination
  • Symptoms: LOC, dilated, nonreactive ipsilateral (same side) pupil)
  • Brief loss of concusnious then says ok then goes into deep sleep and dies
  • Always lense looking picture (bubble under screen protector)
  • Pupil does not match motor response

collection of blood between the inner skull and the outermost layer of the dura, most often associated with skull fractures and middle meningeal artery lacerations or skull fractures with venous bleeding

41
Q

Subdural hematoma –

A
  • Venous bleed
  • May be acute, subacute, or chronic
  • Symptoms: LOC or any neurological deficit
  • Easier to control
  • Acute come to hospital w/in 24 hrs

accumulation of blood between the dura and underlying arachnoid membrane, usually related to a rupture in the bridging veins between the cerebral cortex and the dura

42
Q

How would you care for hematoma patients?

A

Monitor LOC, maintain airway and ventilation, monitor fluid and electrolyte balances, promote adequate nutrition, prevent injury, maintain body temperature, maintain skin integrity, maintain HOB 30 degrees, maintain head and neck in neutral alignment, support family coping, monitor and manage for changes in ICP, CPP and MAP

43
Q

What is the significance of a basilar skull fracture?

A

• Fracture through the base of the skull
• Anterior, middle, or posterior fossa
• High risk for complication of ventral nervous system infection
• The nurse will be the one to see it
The nurse will see the signs of raccoon eyes and battle signs on the patient. You will see CSF otorrhea and CSF rhinorrhea

44
Q

Temporal skull fracture?

A

The temporal lobe lies beneath the temporal bone, a strong blow to the head the temporal lobe is easily contused and lacerated as it moves against its hard irregular surface. This lobe has the primary function of hearing, speech, behavior, and memory. Seizures in this area cause auditory, visual, and sensory hallucination.

45
Q

What is Racoon’s sign?

A

Subconjunctiveal and periorbital ecchymosis

46
Q

Battle’s sign?

A

Ecchymosis overlying the mastoid process behind the ear

47
Q

What is a cerebral aneurysm?

A

Weakened areas in the wall of a blood vessel that causes the blood vessel to bulge a balloon out in the brain

48
Q

What are potential problems for a patient with a cerebral aneurysm?

A
  • Cerebral vasospasm
  • Fluid / Electrolyte imbalances
  • Hydrocephalus
  • ICP
49
Q

What is a subarachnoid hemorrhage(SAH)?

A

bleeding into subarachnoid space, caused by rupture of cerebral aneurysm or arteriovenous malformation (AVM) resulting in diffuse pattern of bleeding

50
Q

What are s/s of SAH?

A
  • “the worst headache of my life”
  • sentinel hemorrhage or warning headaches in the weeks before the SAH
  • Transient loss of consciousness
  • Nausea/vomiting, blurred vision
  • Photophobia
  • Seizures
  • Nuchal rigidity (pain when flexing neck)
  • Restlessness
  • Diminished level of consciousness – even if answer correctly but if have to think about it is a change in LOC
  • Focal neurological signs related to the vascular territory involved in the hemmorrage
  • Cranial nerve deficits (especially II, IV, or VI)
  • Cushing’s triad –
  • Elevated SBP
  • Widening pulse pressure – so > 40
  • Bradycardia
51
Q

Initial Management of Patient SAH

A
  • Admit to ICU
  • ABC’s
  • Possible central/swan-ganz/arterial line
  • Possible external ventricular drain (EVD)
  • Strict blood pressure management – differ ischemic vs hemoraghic
  • Nimodipine (Nimotop) – reduces vasospasm and control bp, given every 2 hours no matter what
  • Medical Management
  • Stool softeners
  • Ulcer, seizure, and DVT prophylaxis
  • Cannot protect their own airway
  • If GCS is 8 or less then intubate immediately
  • Warm, dry, adequate pulse, and good color then good CO
  • Don’t put drain in if not enough CSF
52
Q

Prevent Rebleeding with SAH

A
  • Rebleeding rate – 4% of SAH in first day; 15-20% within 14 days
  • Strict bp control
  • SAH precautions
  • Close monitoring
  • Quiet, dark room accommodations
  • Analgesia for pain and headache
  • Limitation of visitors
  • Give pain meds but not so much that masks pain, need to chart the pain
53
Q

Endovascular Procedures for SAH

A

Coil
• very thin, microscopic gold thread
• go in through groin and feed coil up to aneursym
• packing aneurysms
• keeps blood from going up
• watch for: bleeding in leg, retroperitineal bleed
• check pulses/vitals every 15 mins 1st hours then every 30 mins
• make sure to check CO – color, pulse
• nuero checks very important any change in LOC
• before: take off metformin, see if they are allergic

important that pt understands the informed consent of both clip and coil

54
Q

Surgical Intervention for SAH

A
  • a craniotomy is performed

* a clip is placed across the neck of the aneurysm

55
Q

Nursing SAH

A
  • airway management
  • vital signs/neuro checks q15 mins
  • pain control
  • fluid management
  • management of maintenance IV access
  • observation (after coiling) for bleeding at site
  • loss of pulse to extremity
  • back pain
  • decreased U/O
  • vomiting
  • tachycardia or hypotenstion
56
Q

What is the MOA/indication of the medication nimodipine (Nimotop)?

A

–It’s a calcium channel blocker that is used for the cerebral vessels and it causes vasoconstriction to help with the aneurysm bleeding
reduces vasospasm and control bp, given every 2 hours no matter what
inhibits the transport of Ca into vascular smooth muscle cells, resulting in inhibition of excitation- contraction coupling and subsequent contraction

Critical Care Exam 4 (4 decks)

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