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NSG 478 > Care of Acute Neuro Patients > Flashcards

Care of Acute Neuro Patients Flashcards

1
Q

Cerebrum

A
  • Frontal-concentration, abstract thought, information storage/memory, motor function
  • Broca area-motor control of speech
  • Parietal-analyzes sensory data
  • Essential to awareness of body position in space, size and shape discrimination, right and left orientation
  • Temporal-auditory receptive areas; memory of sound, understanding language and music
  • Occipital-visual interpretation and memory
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2
Q

Midbrain

A

center for auditory and visual reflexes (CN III, IV originate)

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3
Q

Pons

A

helps regulate respiration (CN V-VIII originate)

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4
Q

Medulla

A

Reflexes: respiration, BP, HR, cough, vomiting, swallowing, sneezing
(CN IX-XII originate)

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5
Q

Cerebellum

A

provides smooth controlled movement; controls fine movement, balance, and proprioception (positional sense, awareness of position of extremities without looking at them)

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6
Q

Normal CSF charecteristics

A
  • Clear color
  • Low specific gravity (Thin liquid), 1.007
  • Protein
  • Glucose, is present a glucose test can be used to confirm
  • WBC minimal (If WBC are present this can indicate an infection)
  • No RBC (its clear)
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7
Q

Art blood supply of the brain

Probably dont need to know

A

Common Carotid Artery Internal Carotid Arteries Anterior(ACA) and Middle (MCA) Cerebral Arteries Anterior and Posterior Communicating Arteries form Circle of Willis

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8
Q

Circle of Willis

A

Frequent site of brain aneurysms, if left untreated it can lead to death easily

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9
Q

Cranial nerve I

A

Olfactory
* Sensory
* Smell

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10
Q

Cranial nerve II

A
  • Optic
  • Sensory
  • Vision: Tested by visual acuity and vision fields
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11
Q

Cranial nerve III

A
  • Oculomotor
  • Motor
  • Pupil reflex, eyelid elevation and eye muscle movement (EOMs); test pupils with light, squeeze eyes shut then open, test eye movement upper outer, upper inward and medial

PERRLA: Pupils, Equal, Round, Relective to light, Accommodation

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12
Q

Cranial nerve IV

A
  • Trochlear
  • Motor
  • Down and inward movement of the eye
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13
Q

Cranial nerve V

A
  • Trigeminal
  • Both
  • M: Jaw movement, chewing and clench cheeks
  • S: Face and neck sensation, light touch and temp
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14
Q

Cranial nerve VI

A
  • Abducens
  • Motor
  • Lateral eye movement
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15
Q

Cranial nerve VII

A
  • Facial
  • Both
  • M: Raise eyebrows, smile, show teeth, puff out cheeks
  • S: Taste on anterior 2/3 of tongue
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16
Q

Cranial nerve VIII

A
  • Acoustic
  • Sensory
  • Hearing
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17
Q

Cranial nerve IX

A
  • Glossopharyngeal
  • Both
  • M: Pharyngeal movement and swallowing, gag reflex, ability to swallow, uvula elevating with a
  • S: Taste on posterior 1/3 of tongue
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18
Q

Cranial nerve X

A
  • Vagus
  • Both
  • M/S: Swallowing and speaking
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19
Q

Cranial nerve XI

A
  • Accessory
  • Motor
  • Shoulder muscle movement, shrugging
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20
Q

Cranial nerve XII

A
  • Hypoglossal
  • Motor
  • Tongue movement and strength

Tongue should be midline

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21
Q

Altered level of consciousness:

A

Reduced state of wakefulness, awareness or alertness to stimuli

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22
Q

Minimally conscious state

A

Patient has inconsistent but reproducible signs of awareness

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23
Q

Coma

A

Clinical state of unarousable unresponsiveness with no purposeful movements or responses to internal or external stim

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24
Q

Patho for altered LOC

A
  • Caused by dysfunction of cerebral hemispheres, cells in nervous system or neurotransmitters in the RAS
  • Can be caused by stroke, toxicity, infection, or metabolic causes
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25
Q

Reticular Activating system (RAS)

A
  • Responsible for wakefulness/sleep wake cycle, attention, ability to focus, arousal, muscle tone
  • Located in hypothalamus and brainstem
  • Vascular supply from circle of willis
  • Receives input from spinal cord, sensory pathways, thalamus and cortex
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26
Q

Causes of altered LOC: Trauma

A
  • Stroke
  • Head Injury
  • Cerebral bleed
  • Tumor
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27
Q

Causes of altered LOC: Toxic

A
  • Drug overdose
  • Alc intox
  • Carbon monoxide
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28
Q

Causes of altered LOC: Infection

A
  • Meningitis
  • Encephalitis
  • Brain abscess
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29
Q

Causes of altered LOC: Metabolic

A
  • DKA
  • Hepatic or renal injury or failure
  • Hyponatremia
  • Hypoxia
  • Seizures
  • Heat stroke
  • Hypothermia
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30
Q

Ways to assess changes in LOC

A
  • Glascow coma scale (3-15)
  • Cranial nerves
  • Cerebellar function: Balance and coordination
  • Reflexes: Gag,pupils, DTR, Babinski
  • Motor function: Muscle strength
  • Sensory function: Ability to feel temp (warm and cold, sharp/light touch or vibration)
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31
Q

Babinski reflex

A
  • Normal for adults: Stroke from heel to toes, the toes should crunch down
  • Abnormal: Stroke from heel to toes, the toes spread and go up
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32
Q

GCS: Eye opening response

A

4.) Eyes open spontaneously
3.) Eyes open to commands
2.) Eyes open to pain
1.) No eye opening

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33
Q

GCS: Motor response:

A
  1. None
  2. Decerebrate posturing
  3. Decorticate posturing
  4. Withdrawal from pain
  5. Purposeful movement to pain (Bats at your hand)
  6. Obeys commands
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34
Q

GCS: Verbal

A
  1. None
  2. Incomprehensible: Grunts or non words
  3. Inappropriate: words are discernible
  4. Confused: but able to answer questions
  5. Orientated
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35
Q

What’s worse decor or decerb

A

Decerb

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36
Q

Blood Work for altered LOC

A
  • CMP: Electrolytes, glucose, calcium, liver function, kidney function, serum osmolality
  • CBC with diff: Noting abnormally high or low counts (Infection)
  • Coagulation studies (PT/INR/ PTT), (Can be hypoxia from anemia)
  • Ammonia level (hepatic encephalopathy)
  • Ketones (DKA)
  • Tox screen (Drugs)
  • ABG
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37
Q

Serum osmolality

A

Really good at telling us the fluid status

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38
Q

Imaging for altered LOC

A
  • CT/MRI
  • No lumbar puncture in suspected increase in ICP, can cause brain herniation
  • Perfusion CT: See vasculature
  • MR Spectroscopy: Can identify location of tumor stroke, epilepsy
  • EEG: detects abnormal brain waves
  • PET: Shows metabolic changes
  • SPECT: Shows a detailed 2d map of the brain
  • Cerebral angiogram: assess brain vasculature
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39
Q

Medical mgmt of altered LOC: Airway

A
  • Pt intubated vs tracheostomy needed
  • Can the pt protect their own airway
  • Mechanical ventilation until determined

Done first

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40
Q

Medical mgmt of altered LOC: Circulation

A
  • BP, HR: Is it adequate to perfuse body and brain
  • Peripheral IV, ART line, Central line, Pulmonary art cath
  • IV fluids and meds

Done Second

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41
Q

Medical mgmt of altered LOC: Determine the underlying cause

A
  • Determine neuro pathology
  • Treat the underlying cause
  • Prevent complications

Done third

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42
Q

Causes of increased ICP and thus brain herniation

A
  • Space occupying lesion (Tumor, abscess, hematoma, contusion, subarachnoid hemorrhage
  • Generalized brain swelling (Liver failure (Hepatic encephalopathy) hypertensive encephalopathy)
  • Increased venous pressure (HF, obstruction of the superior mediastinal veins or jugular veins, venous thrombosis,)
  • Obstruction of CSF flow (Hydrocephalus, meningeal disease)
  • Increased production of CSF

Monro-kellie doctrine

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43
Q

Cerebral Edema

A

Swelling of the brain resulting in an increase in volume of brain tissue

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44
Q

Autoregulation

A
  • Brain’s ability to change the diameter of its blood vessels to maintain consistent CBF during alterations in systemic BP
  • Normally its in a state of equilibrium (CSF, Blood brain tissue)
  • Mechanism: Shift or displacement of CSF, increased absorption or decreased production of CSF, decreased cerebral blood volume
  • Occurs constantly based on changes in intrathoracic pressure (Coughing sneezing straining), posture, BP O2 and CO2 levels
  • CAN BECOME IMPAIRED WITH PATHOLOGIC AND SUSTAINED INCREASED ICP
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45
Q

Monro-Kellie Hypothesis/Doctrine

A
  • Essentially the skull vault is composed of 3 things, brain, blood and CSF, if one of those increase and the others don’t decrease you’re gonna have a hemorrhage
  • If one of these increase it causes a change in the volume of one or both components.
  • Loss of autoregulation;normal mechanisms exhausted; increased ICP and decreased cerebral blood flood -> Brain injury, ischemia and cell death
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46
Q

Normal ICP

A

0-15 mmHg

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47
Q

Normal Cerebral Perfusion Pressure (CPP)

A

70-100 is ideal
Above 60 is ok
Below 50 is bad

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48
Q

At what CPP does irreversible brain damage occur

A

Below 50 mmHg

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49
Q

How to calculate CPP

A

MAP-ICP
Indicates the pressure which blood has to flow against in the skull which limits perfusion to the brain

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50
Q

Cushing’s Triad

A
  • Increase in SBP (widening Pulse pressure)
  • Decrease in HR
  • Decrease in RR
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51
Q

Cushing’s Response

A
  • Nervous system response to acute elevation in ICP
  • Autoregulation becomes ineffective
  • Changes in mental status occur
  • Vital signs change as well (Cushing’s triad)
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52
Q

Decreased CPP leads to

A

Cerebral ischemia, infarction, brain death

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53
Q

Pulse pressure

A
  • Difference between the systolic and diastolic bp
  • Not the same thing as MAP
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54
Q

MAP

A
  • Mean arterial pressure
  • Average art pressure in one cardiac cycle, varying due to CO and SVR
  • (2DBP+SBP)/3
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55
Q

Herniation

A
  • Life threatening event which an area of the brain exits the skull vault through one of the rigid intracranial barriers
  • Classified based on structure it exits through
  • Path of least resistance, with a build up of pressure in the skull the brain has to go somewhere
  • CT of the brain showing a midline shift indicates URGENT intervention

monro kellie

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56
Q

S+S of increased ICP+ impending herniation: Pre-herniation

A
  • HA, Vomiting
  • Changes in LOC (restless agitation, confusion, increased sleepiness), high highs low lows
  • Cushing triad
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57
Q

S+S of increased ICP+ impending herniation: Herniation

A
  • Dilated, fixed unilateral pupils (Blown pupil) or fixed bilateral unequal pupils
  • Decorticate or decereberate posturing
  • Oculomotor paresis (EOM)
  • Homonymous hemianopia- visual field cut
  • Hemiparesis
  • Loss of reflexes: Oculocephalic, oculovestibular, corneal
58
Q

Treatment, increased ICP/herniation: Goals

A
  • Identify increased ICP early, prevent dmg
  • Relieve increased ICP
  • Decrease Cerebral edema
  • Lower volume of CSF
  • Decrease Cerebral blood flow
  • Maintain cerebral perfusion
59
Q

Treatment: Increased ICP/herniation

A
  • Oral intubation, avoid nasotracheal intubation
  • Correct blood pressure, maintain CPP to 60-70
  • Place ICP Monitoring device and ART line
60
Q

Why do you avoid nasotracheal intubation for increased ICP

A
  • Increases coughing, gagging, which increases intrathoracic pressure which in turn increases ICP
61
Q

Methods to monitor ICP: Intraventricular cath

A
  • Gold standard
  • Connected to drainage bag for excessive CSF drainage
  • Complications: Infection, hemorrhage during placement, difficult to place with small ventricles, ventricular collapse, occluded cath
62
Q

Methods to monitor ICP: Intraparenchymal

A
  • Thin cable with electronic or fiber optic transducer at tip placed directly on the brain parenchyma through a burr hole on the skull
  • Lower risk of infection, hemorrhage and easier to place
  • Cons: Cannot drain csf, can lose accuracy over time and mechanical failure due to complex design
63
Q

Methods to monitor ICP: Subarachnoid

A
  • Bolt with fluid coupled system, hollow screw placed through skull, dura punctured and CSF communicates with the fluid column and transducer
  • Lower risk of infection and hemorrhage
  • Cons: Can clog with debris, unreliable, and less accurate
64
Q

Methods to monitor ICP: Epidural

A

Optical transducer that rest against the dura, often inaccurate, limited use

65
Q

When are ICP monitoring devices typically used

A

When no reliable neuro exam can be performed due to sedation, anesthesia, low GCS (<9)

66
Q

Mild GCS score

A

12-15

67
Q

Moderate GCS score

A

9-12

68
Q

Severe GCS score

A

3-8
Comatose

69
Q

ICP monitoring equipment: Calibrating a transducer

A
  1. Zeroed to atmospheric pressure at the level of the tragus (Level of the foramen of monro) and leveled with a 0 mark on the drainage bag
  2. Drain set at a specific height above tragus for drainage (15cm H20); So when ICP exceeds that amount it will drain off
  3. Always level transducer for position changes (T+P)
  4. Ensure all connections are secure and no leakage of fluids (Infection risk as its connected directly to the brain)
70
Q

Treatment for increased ICP: Methods to control ICP

A
  • Maintain an ICP goal of <20 mmHg
  • Remove CSF via a ventriculostomy
  • Elevate HOB 30 degrees to enhance cerebral venous drainage and keep head and neck midline, avoid neck rotation and flexion
  • Sedation (Control agitation pain and excessive muscular activity, which all increase ICP)
  • Hypervent (Decreases PaCO2, goal is 26-30 only really used in emergency
  • Hydration: Maintain Euvolemic state (Isotonic fluids only .9%)
    • restrict oral free water
    • No .45% NS or DSW because they contain more water
  • Keep osmolality 295-305 (High and dry)
  • Mannitol to decrease cerebral edema and ICP (Osmotic diuretic)
  • Keep CPP greater than 60 (Use vasopressors not fluids)
  • Antihypertensives only in cases of severe HTN (180/95) and only if they are able to maintain their CPP
  • Corticosteroids: Used for edema for Tumor or infection only
  • Minimize suctioning (Increases ICP)
  • Avoid valsalva maneuver (Stool softeners)
  • Treat the fever (increases metabolism, which increases ICP) maintain normothermia
  • Anticonvulsants
71
Q

Mgmt of increased ICP: Normal measures fail

A
  • Hypothermia (Controversial, don’t want them to shiver)
  • Pentobarbital coma: Decreases metabolic command
  • Decompressive craniectomy: Cut a chunk of skull off so the brain can expand
72
Q

Mgmt of increased ICP: mgmt of underlying cause

A
  • Remove blood clot
  • Resect tumor
  • Divert CSF if hydrocephalus
  • Treat metabolic disorder
73
Q

Mgmt of increased ICP: Supportive measures

A
  • Vent support
  • Seizure prevention
  • F/E maintenence
  • Nutrition
  • Skin care
  • Pain and anxiety
  • Oral cvare
  • Monitor for infection
74
Q

ICP waveforms

A
  • Should have 3 peaks
  • P1-P3
75
Q

ICP waveforms: P1

A
  • Percussion wave due to art pulsation
  • It represents SBP
  • Should be the tallest wave
76
Q

ICP waveforms: P2

A
  • Represents brain compliance, tidal wave
  • If P2 is greater than P1 there is increased intracranial volume and pressure, decreased brain compliance Impending herniation
77
Q

ICP waveforms: P3

A
  • Dicrotic wave
  • Aortic valve closure
78
Q

Lundberg waves on ICP tracing: Lundberg A waves

A
  • Plateau waves
  • Transient, recurring elevations in ICP
  • Lasting 5-10 min
  • Ranges 40-100 mmHg
  • Indicates changes in volume, early cerebral perfusion compromise
  • Decreased brain compliance, impending herniation

Very bad

79
Q

Lundberg waves on ICP tracing: Lundberg B waves

A
  • Last 30 sec-2 min
  • Unclear value in clinical practice
  • Normal
80
Q

Lundberg waves on ICP tracing: Lundberg C waves

A
  • Small rhythmic oscillations
  • 4-8 per min
  • Appear related to rhythmic variations in art BP and resp
81
Q

Other Neuromonitoring: SjvO2

A
  • Oxy sat in jugular venous bulb or vial cath in brain
  • Can identify changes in cerebral oxygenation
  • Desaturations can reflex early cerebral ischemia before increase in ICP occurs
  • Can improve outcomes
  • Reflects overall brain perfusion no specific injured area
82
Q

Other Neuromonitoring: Fiberoptic cath in parenchyma

A

Monitors oxy and temp

83
Q

TBI: Four primary mechanisms

A
  • Direct impact
  • Sudden or rapid acceleration and decelerations
  • Penetrating injury
  • blast injury
84
Q

TBI: Primary injury

A
  • Consequence of direct contact to the head or brain during initial injury
  • External: Contusion, lacerations, external hematomas, skull fractures
  • Intracranial: Subdural hematoma, concussion, diffuse axonal injury
85
Q

TBI secondary injury

A
  • Evolves over hours and days after initial injury due to lack of glucose and oxygen deliver to the cells
  • Intracranial: Hemorrhage, cerebral edema, intracranial hypertension, hyperemia, seizures, vasospasm
  • Systemic: hypotension, hyperthermia, hypoxia, hypercarbia, infection, electrolyte imbalances, anemia
86
Q

TBI: What can occur after the injury

A
  • Cerebral edema: cerebral hypoxia and ischemia, cerebral metabolic impairment, cerebral vasospasm, increased intracerebral pressure
  • Cell death
  • Increased glutamate
  • Mitochondrial dysfunction, impairment of glucose metabolism
  • Blood brain barrier dmg
  • Excitotoxicity
  • Complement activation and inflammation and ROS generation
87
Q

TBI: Skull fracture, skull base

A
  • Causes persistent localized pain
  • Can produce hemorrhage from nose, pharynx or ears
    • Battle sign, racoon eyes
    • Basal skull fracture: suspected when csf escapes from the ears and nose
      • Risk for meningitis due to open dura
      • Csf is clear, very watery
      • Test for beta 2 transferrin, collect in a small tube
88
Q

Mgmt of skull fracture: Non-depressed

A

Close observation

89
Q

Mgmt of skull fracture: Depressed

A

Surgery to elevate the skull and debridement

90
Q

Closed TBI

A
  • Head accelerates then rapidly decelerates or collides with another object
  • Causes brain tissue dmg but no open dura
91
Q

Open TBI

A

Object penetrates the skull, entering the brain through the dura and dmgs the brain tissue

92
Q

TBI types: Concussion

A
  • Temp loss of neuro function without apparent structural dmg to the brain
    • Mgmt: Observation and prevent secondary injury
    • Monitor for changes in LOC worsening HA dizziness, seizure, abnormal pupil response, vomiting irritability, slurred speech, numbness or weakness in arms or legs
    • Repeat concussions lead to chronic traumatic encephalopathy
93
Q

Diffuse axonal injury

A

Terrible, involves the shearing of nerve fibers as the brain rotates in the skull

94
Q

TBI Types: Intracranial hemorrhage

A
  • Hematoma in the brain
  • Epidural: above the dura
  • Subdural: Below the dura
  • Intracerebral: Within brain
  • S+S depend on how slow or quick the hematoma expands and compresses tissue
95
Q

TBI Types: Intracranial hemorrhage, Fast bleed

A

Can be fatal, due to the brain having no time to compensate
Typically do worse

96
Q

TBI Types: Intracranial hemorrhage: Slow bleed

A

Generally do better than a fast bleed due to there being time for the brain being able to compensate

97
Q

TBI Types: Epidural hematoma (EDH)

A
  • Between the skull and the dura
  • Aften due to laceration of meningeal artery from skull fracture
  • Hemorrhage causes rapid pressure on the brain
  • Medical emergency: Surgery to make a burr hole or craniotomy to decrease ICP, remove clot, control bleeding, placement of a drain to prevent accumulation of blood
98
Q

Epidural hematoma S+S

A
  • Brief loss of consciousness, but then awake
  • Lucid, conversant but then increased restlessness, agitation, confusion, signs of herniation
99
Q

TBI Types: Subdural Hematoma (SDH)

A
  • Collection of blood between the dura and brain
  • Often venous in origin
  • Acute or chronic depending on size of vessel and amount of bleeding
100
Q

Subdural Hematoma: Acute SDH

A
  • Usually due to a fall
  • S+S: Change in LOC, Pupil changes, hemiparesis
  • Increased BP, Decreased HR/RR, comatose indicates a rapidly expanding hematoma
  • Treatment needs emergent craniotomy to remove the clot
101
Q

Subdural hematoma: Chronic SDH

A
  • Brain has time to compensate
  • Hematoma develops slowly, weeks to months
  • Brain atrophied so there is more room to expand
  • Blood changes characteristics in 2-4 days, becoming thicker and darker
  • Brain adapts to this and you can see fluctuating neuro, personality changes, mental deterioration, focal seizures
  • Mgmt: Surgical evacuation of the clot (Burr holes or craniotomy)
102
Q

TBI Types: Intracerebral Hemorrhage/Hematoma

A
  • Bleeding into the parenchyma of the brain
  • Usually due to force exerted over small area of head (Missiles, bullets, stabbing)
  • S+S: INsidious, headache, neuro changes
  • Treatment: Supportive care, ICP control, careful fluid mgmt, lyte monitoring , antihypertensives
    • Surgery: Craniotomy, craniectomy to remove clot and control hemorrhage
    • Site may not be accessible or lack of clearly defined margin prevents removal of clot
103
Q

TBI Types: Diffuse axonal injury

A
  • Due to severe head injury
  • From widespread shearing and rotational forces that produces dmg through the brain
  • Damage is diffuse across the entire brain
  • Poor prognosis: recovery depends on severity of injury
  • No awake, lucid period; patient is coma immediately with posturing (Decor/decerb) and global cerebral edema
  • Can have prolonged coma
104
Q

Mgmt of TBI: Assessment

A
  • MRI/CT
  • Assume cervical spine injury until ruled out
    • Transported on a board with head and neck aligned in neutral position
    • Cervical collar
    • C-spine Xrays
105
Q

Mgmt of TBI: Goals

A
  • Preserve brain homeostasis and prevent secondary injury
  • Cerebral edema after TBI peaks 48-72 hours after injury
106
Q

Mgmt of TBI: Causes of secondary injury

A
  • Cerebral edema
  • Hypotension
  • Respiratory depression
  • Hypoexmia
  • F/lyte imbalance
107
Q

Mgmt of TBI:Treatment

A
  • Stabilize ABC
  • Maintain CPP
  • ICP mgmt
  • Control hemorrhage
  • Maintain optimal ABG
  • Fluid and electrolyte balance
  • Maintain proper positioning to promote venous drainage
  • Seizure prophylaxis
  • Manage pain and anxiety and agitation
  • NG tube: prevent regurg/aspiration
108
Q

Neuro mgmt of TBI and Coma: Initial injury

A
  • When did injury occur, what caused it, direction and force of the blow
  • Loss of consciousness at time of injury and for how long, was the pt arousable
109
Q

Neuro mgmt of TBI and Coma: Neuro checks

A
  • Done at least every hour
  • GCS to determine LOC
  • Assess motor function compare all extremities and L/R on command, speech and noxious stim
  • Pupils- Bilateral, sluggish, brisk to light, equal size or unequal
  • Behavior-Emotional lability, aggressive, uninhibited
  • Document thoroughly
  • Notify provider of changes immediately
110
Q

Anisocoria

A

Pupils unequal

111
Q

Monitor VS for changes related to increased ICP, Early signs

A
  • Cushing triad: Bradycardia, systolic hypertension, widening pulse pressure, resp depression
112
Q

Monitor VS for changes related to increased ICP: Later signs

A

Bradycardia, Hypotension, tachypnea

113
Q

Monitor VS for changes related to increased ICP: Hyperthermia

A
  • Maintain a temp under 100.4/38c (Increased temp increased metabolic demand on the brain
  • Fever may indicate brain stem dmg
  • Don’t want them to shiver either as that can increase ICP
114
Q

Neuro mgmt of TBI and Coma: S+S of increased ICP and CPP

A
  • Know elevated ICP mgmt
  • Proper position of head and body
115
Q

Neuro mgmt of TBI and Coma: Anticonvulsants

A
  • Drug level monitoring, need to maintain a therapeutic range
  • Side effects
116
Q

mgmt of TBI and Coma: Respiratory

A
  • Airway: Maintain the airway, is the patient able to protect their own airway, if no they getting tubed
  • Oxygen sat and pulse ox
  • ABG: hypoxemia, hypercarbia, brain sensitive to hypoxia and deficits can worsen if hypoxic
  • Lungs sounds: Present? clear or adventitious?
  • Resp pattern: Regular irregular (Unless vented) cheyne stokes
  • RR: Low normal or high?
  • Cough reflex intact or absent: guard against aspiration, check cuff on ett or trach
  • CBC: Anemia HH plt function, WBC
  • Chest X-ray: Atelectasis, contusion, pneumothorax, neurogenic pulmonary edema
  • Sputum cultures
  • Minimize suctioning if increased ICP as it can increase ICP: If needed make it should
  • Monitor for ARDS, pneumonia , fluid overload
  • Good oral hygiene to help prevent against vent associated pneumonia
  • PEEP, use cautiously can increase intrathoracic pressure increasing ICP
117
Q

mgmt of TBI and Coma: Cardiovascular

A
  • Assess vitals: HR+BP
  • Monitor for and treat arrhythmias: Determine the underlying cause
  • BP mgmt
    • IV fluids vs vasopressors, vasopressors are better
    • Manipulate CO to maintain adequate CPP
    • Maintain good MAP
    • Maintain CPP (60-70)
  • Monitor for venous thromboembolism (DVT and PE)
  • 12 lead ECG: Ischemia/ infarction
118
Q

mgmt of TBI and Coma: Lyte and fluids

A
  • Want to maintain normal levels
  • Strict I+O
  • Daily weight
  • Serum and urine electrolytes
  • Glucose level
  • Serum osmolality
  • Urine specific gravity and ketone
  • Monitor skin turgor and mucous membranes
119
Q

mgmt of TBI and Coma: Lytes and fluid monitoring for

A
  • Hyponatremia
  • Effects of osmotic diuretic
  • Diabetes insipidus (DI)
  • SIADH
  • Hyperglycemic hyperosmolar syndrome
120
Q

mgmt of TBI and Coma: Lytes and Fluids interventions

A
  • Correct hyponatremia: Fluid restriction 3% hypertonic saline Do not correct rapidly increase by 4-6 mEq/L over 24 hours
  • Correct Hypokalemia
  • Insulin for hyperglycemia
  • If giving mannitol, monitor for pulmonary edema and HF (Fluid staying in vasculature rather than excreted), want to see increased urine output
121
Q

mgmt of TBI and Coma: GI

A
  • Monitor and prevent ileus
    • Bowel sounds and abd distension
  • Nutrition early: improves outcomes and prevents ileus
    • Enteral feeds: NG, NJ PEG
    • Needs an active bowel to be used (Bowel sounds and no ileus)
    • HOB up to prevent aspiration
    • High cal high protein
  • TPN: not usually prefered
  • Constipation mgmt: From bed rest, NPO, fluid restrictions, pain meds
  • Bowel incontinence
    • Altered LOC
    • SKin care
  • GI bleeding prophylaxis (Basically everyone needs this)
    • PPI
    • Monitor for bleeding (Change in stool color, decreased H+H, gastric aspirate)
122
Q

mgmt of TBI and Coma: GU

A
  • Diuretics
    • Strict I+O
    • Mannitol
    • Monitor fluids and lytes
  • Incontinence
    • Skin care
    • Foley cath, condom cath
    • Monitor for infection
123
Q

mgmt of TBI and Coma: Musculoskeletal

A
  • Assess ROM, development of deformities or spasticity
  • Passive ROM
  • PT/OT
  • Splints: Hands feet and ankles
  • Proper positioning of patient with increased ICP
    • HOB 30 degrees
    • Minimal elevation of legs
    • Head and neck aligned neutrally
124
Q

mgmt of TBI and Coma: Integumentary

A
  • Assess skin integrity and oral mucosa q8 hrs or more frequently
  • Assess under trach collar or ties or et tube
  • Turn and position Q2 hrs
  • OOB to chair 3x daily if able
  • Early ambulation if able
  • Skin care per institution policy
    • Allevyn
    • Speciality bed
  • Frequent oral care
    • Minimizes infection risk
    • Monitor for breakdown of lips from ET tube
    • Lubricant for lips
125
Q

mgmt of TBI and Coma: Agitation and restlessness, causes

A
  • initial brain injury
  • Emerging from coma
  • Increasing ICP
  • Fever
  • Hypoxia
  • Pain/discomfort
  • Full bladder
  • Restraints
126
Q

mgmt of TBI and Coma: Preventing injury/ problem solving in agitated/ restless pt

A
  • Ensure oxygenation is adequate, bladder not distended, dressings, cast, splints not constricting flow
  • Padded side rails
  • Wrap hands so they cannot pull out tubes and to prevent self injury, avoid restraints
  • Speciality bed, bed is at floor level
  • Reduce stimuli
  • Adequate lighting
  • re-Orientate pt
  • Avoid opiates to control restlessness/agitation
  • minimize disruption in sleep wake cycle, cluster nursing care , lights on, shade open, dark in evening
  • Limit waking pt if able
  • Keep sheets dry if incontinent
127
Q

mgmt of TBI and Coma: Fever causes

A

Due to hypothalamic dmg
cerebral irritation
hemorrhage
infection

128
Q

mgmt of TBI and Coma: Interventions

A
  • Check temp every 2-4 hours (Continuous thermometer)
  • Identify cause of fever
  • Treat with acetaminophen and cooling devices
  • Maintain normothermia
  • Do not cause shivering: Increases ICP and metabolic demand
  • Culture blood urine and sputum
  • Antibiotics as prescribed
129
Q

mgmt of TBI and Coma: Post TBI seizures

A
  • Can occur immediately (within 24 hours) early (1-7 days ) or late (7+ days)
  • Causes increased ICP and decreased oxygenation
  • Admin anticonvulsant prophylaxis
  • Can be weaned off once past acute phase unless had a seizure
130
Q

Complications of increased ICP: Brain stem herniation

A

Increased pressure creates downward pressure of the brain stem, resulting in cessation of blood flow to the brain, causing irreversible anoxia and brain death

131
Q

Complications of increased ICP: DI

A
  • Due to decreased secretion of ADH, from pituitary
  • Makes you pee a ton, decreasing urine osmolality and serum hyperosmolarity
  • Urine is clear
  • Mgmt: IV fluids, electrolytes, Vasopressin DDAVP

Dehydration is major concern

132
Q

Complications of increased ICP: SIADH

A
  • Excessive ADH secreted
  • Stops you from peeing, volume excess
  • Serum Na is dilute as a result of the volume excess
  • Treated with fluid restriction with no free water and in severe cases 3% saline
133
Q

Hallmark of brain death

A
  • The person is dead when the brain is dead
  • Zero possibility of recovery
  • Needs to be verified by 1-2 physicians
  • Pt needs to be
    • Removed from sedation, neuromuscular blocking agents CNS depressants
    • Normal body temp (36 degrees)
    • SBP over 100 (Can use vasopressors)
    • No sevre lyte, acid base or endocrine disturbances
134
Q

3 cardinal signs of brain death

A
  • Coma
  • Absence of brain stem reflexes
  • Apnea
135
Q

3 cardinal signs of brain death: Coma

A

Complete loss of consciousness

136
Q

3 cardinal signs of brain death: Absence of brain stem reflexes

A
  1. Pupillary reflex: Pupils are fixed, mid size or dilated not reactive to light
  2. Corneal reflex: Drop of saline in the eye, person should blink if not its absent
  3. Oculovestibular reflex: Irrigate each ear canal with ice water, absent if the eyes do not move to irrigated ear within 1 min
  4. Gag Reflex
  5. Cough reflex: Person coughs when suctioning
  6. Occulocphalix reflex: Hold eyes open, turning head side to side, normally the eyes turn in opposite side the head is turning
137
Q

3 cardinal signs of brain death: Apnea

A
  • Removal from vent with no spontaneous breaths
  • Preoxy 100% for 10 min, vent 10 bpm Peep is 5 cmH20 if SPO2 >95 do abg, disconnect from vent continue with O2 100% 6l through ETT
  • Monitor for rep movements for 8-10 min , if none do an ABG at 8 min
  • If no respirations and PCO2 is >60 mmHg apnea test is positive
138
Q

Ancillary test brain death:

A
  • Cerebral angiography-gold standard; confirms absence of blood flow to brain
  • CT angio or MR angio-shows cessation of cerebral blood flow
  • EEG—will show no brain activity
  • Somatosensory evoked potentials (SSEPs): no somatosensory evoked potentials in response to bilateral median nerve stimulation and no brain stem evoked potentials in response to auditory stimuli, can confirm EEG findings
  • Transcranial doppler ultrasound—can assess pulsations of middle cerebral arteries, vertebral and basilar arteries
139
Q

What happens after brain death is determined

A
  • Need to maintain adequate tissue perfusion for potential organ donation
  • If family declines organ donation, cardiopulmonary support is withdrawn
  • Anticipatory grieving of the family help the family understand
  • Organ donation, needs brain death confirmation in order to proceed
  • Need to collab with a lot of other professions in this
140
Q

Nursing mgmt if care is not withdrawn

A
  • Provide proper suctioning of the endotracheal/tracheostomy tube to remove secretionsfrom the airway. This also helpsto prevent blockage of endotracheal or tracheostomy tubes.
  • Clean all the body parts, especially the face, back, and perineal area.
  • Provide dressing to open wounds (if any) and cover them with gauze pieces.
  • Every patient goes through a different situation despite having the same diagnosis. Nurses should manage the patients accordingly.
  • Visualization of patient treatment and prognosis, as well as counseling daily, may slowly help family members cope with the patient’s degrading health status.
  • Change the patient’s position every 2 hours to prevent bedsores.
  • Check the intravenous cannula sites for redness and swelling.
  • Make sure that the “Do not attempt resuscitation order” (DNR) is in place
  • Provide emotional and psychological support to the family and relatives of the patient, as they may deny seeing their loved ones in the end stage.
  • Find out and inform the organ donation center as soon as a patient is declared brain dead.
  • Respect the patient’s cultural and religious backgrounds.
  • Record and report all the procedures that are done for the patient throughout the hospital stay.

NSG 478 (23 decks)

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