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Module 7 (Critical Care) > Multi-System Trauma Pt. 2 (Head Injury and Burns) > Flashcards

Multi-System Trauma Pt. 2 (Head Injury and Burns) Flashcards

1
Q

Skull has what 3 essential components?

A

Brain tissue
Blood
Cerebrospinal fluid (CSF)
enclosed space - rigid vault

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2
Q

The intracellular and extracellular fluids of brain tissue make up approximately ___% of this volume

A

78

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3
Q

Blood in the arterial, venous, and capillary network makes up ____% of the volume

A

12

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4
Q

____% is the volume of the CSF.

A

10

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5
Q

Primary injuryoccurs at the

A

initial time of an injury (e.g., impact of car accident, blunt-force trauma) that results in displacement, bruising, or damage to any of the three components.
- injury on impact

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6
Q

Secondary injuryis the resulting

A

hypoxia, ischemia, hypotension, edema, or increased ICP that follows the primary injury.
- after injury (swelling, hypoxia, HTN)

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7
Q

Secondary injury, which could occur several

A

hours to days after the initial injury, is a primary concern when managing brain injury

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8
Q

cerebral edema

A

increased accumulation of fluid in the extravascular spaces of brain tissue

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9
Q

cerebral edema results in an

A

increase in tissue volume that can increase ICP

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10
Q

Intracranial pressure (ICP)is the

A

hydrostatic force measured in the brain CSF compartment

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11
Q

What maintains the ICP?

A

the balance among the three components (brain tissue, blood, CSF)

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12
Q

Factors that influence ICP under normal circumstances are changes in

A

(1) arterial pressure; (2) venous pressure; (3) intraabdominal and intrathoracic pressure; (4) posture; (5) temperature; and(6) blood gases, particularly CO2levels.

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13
Q

The Monro-Kellie doctrine states that the

A

three components must remain at a relatively constant volume within the closed skull structure
- displaced, the total intracranial volume will not change.
-This hypothesis is only applicable in situations in which the skull is closed. The hypothesis is not valid in persons with displaced skull fractures or hemicraniectomy.

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14
Q

ICP can be measured in the

A

ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer

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15
Q

Normal ICP ranges from

A

5 to 15 mm Hg. *

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16
Q

A sustained pressure greater than 20 mm Hg is

A

considered abnormal and must be treated.*

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17
Q

What component is the first to go down when increased ICP?

A

CSF - swelling and edema

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18
Q

What goes down next after CSF goes down?

A

Blood
because it can not circulate – hypoxia and ischemia

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19
Q

Brain tissue with increased ICP

A

atrophy, herniation of the foramen in the brain stem

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20
Q

Herniation

A

poor prognosis

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21
Q

Cerebral blood flow(CBF) is the **

A

amount of blood in milliliters passing through 100 g of brain tissue in 1 minute**.

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22
Q

The maintenance of blood flow to the brain is critical because the

A

brain requires a constant supply of O2and glucose

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23
Q

brain uses ___% of the body’s O2and 25% of its glucose

A

20

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24
Q

Autoregulationis the

A

automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow during changes in arterial blood pressure (BP).

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25
Q

purpose of autoregulation is to ensure a

A

consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits
- consistent blood to the brain
- will add or remove O2 when needed by vasodilation or vasoconstriction

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26
Q

CBF decreases, and symptoms of cerebral ischemia, such as

A

syncope and blurred vision

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27
Q

High CBF can be affected by
(>150 MAP)

A

cardiac or respiratory arrest, systemic hemorrhage, and other pathophysiologic states (e.g., diabetic coma, encephalopathies, infections, toxicities

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28
Q

Regional CBF can be affected by

A

trauma, tumors, cerebral hemorrhage, or stroke. – lose elasticity (tx with shunt to get fluid out)

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29
Q

CPP =

A

MAP - ICP

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30
Q

CPP

A

force driving blood into the brain, providing oxygen and nutrients
- ensure blood flow to the brain

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31
Q

ICP increased by

A

intracranial bleeding
cerebral edema
tumor

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32
Q

Increased ICP causes

A

collapsed veins
decrease effective CPP
reduces blood flow

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33
Q

primary determinant ofcerebral blood flow

A

CPP

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34
Q

Normal CPP is

A

60 to 100 mm Hg

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35
Q

CPP decreases

A

autoregulation fails and CBF decreases

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36
Q

CPP of less than 50 mm Hg is associated with

A

ischemia and neuronal death.

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37
Q

A CPP of less than 30 mm Hg results in

A

ischemia and is incompatible with life.

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38
Q

Increased ICP S/S

A

change in LOC
HA, vomiting w/ no N
change in speech
Papilledema
Pupillary changes
impaired eye mvmt
Posturing
flaccid
low motor function
seizures
Cushing’s Triad
- no fever or loss of smell

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39
Q

Cushing’s Triad

A

high systolic BP
low HR
altered respiratory pattern (Kussmaul’s, Cheyne-stokes

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40
Q

major complications of uncontrolled increased ICP are

A

inadequate cerebral perfusion and cerebral herniation

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41
Q

Increased ICP mgmt

A

HOB 30
Head midline with towel rolls
Low stimulation environment
Cluster care
Help family understand (hearing is the last to lose)
- Keep calm and let them rest

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42
Q

Cushing’s Triad is a __________ emergency

A

neurological
-ominous development
-rapid fluctuations of VS

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43
Q

brain compression s/s

A

increases, respirations become rapid, the blood pressure may decrease, and the pulse slows further

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44
Q

Pressure-Volume Curve
stage 1

A

high compliance
The brain is in total compensation, with accommodation and autoregulation intact. An increase in volume (brain tissue, blood, or CSF) does not increase the ICP.

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45
Q

Pressure-Volume Curve
stage 2

A

compliance is beginning to decrease, and an increase in volume places the patient at risk of increased ICP and secondary injury.

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46
Q

Pressure-Volume Curve
stage 3

A

significant reduction in compliance. Any small addition of volume causes a great increase in ICP. Compensatory mechanisms fail, there is a loss of autoregulation, and the patient exhibits manifestations of increased ICP (e.g., headache, changes in level of consciousness or pupil responsiveness).
With a loss of autoregulation, the body attempts to maintain cerebral perfusion by increasing systolic BP.
- decompensation is imminent.
- systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and altered respirations.

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47
Q

Pressure-Volume Curve
stage 4

A

ICP rises to lethal levels with little increase in volume
-herniation

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48
Q

Herniation

A

occurs as the brain tissue is forcibly shifted from the compartment of greater pressure to a compartment of lesser pressure. In this situation, intense pressure is placed on the brainstem, and if herniation continues, brainstem death is imminent.

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49
Q

ICP should be monitored in patients admitted with a

A

Glasgow Coma Scale (GCS) score of 8 or less and an abnormal CT scan or MRI

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50
Q

Monitoring ICP types

A

Subdural
Epidural
Subarachnoid
Intraparenchymal
Ventricular- gold standard

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51
Q

Monitoring ICP mgmt

A

labs and VS for infection (hot, flush, and running a fever)
Sterility
Do not change
Central lines
Biopatch

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52
Q

ICP tubing mgmt for nursing

A

Medications in tubing are only by the physician
Mark it off with labels
Watch temp.
Keep control of the tubing and tidy
Monitor and trend
Good oxygenation and in normal ranges with ABG

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53
Q

Interprofessional CARE for ICP

A

Identify and treat the underlying cause
Support brain function
- O2, ETT/VENT, ABG
Drug therapy
Nutritional therapy

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54
Q

The underlying cause of increased ICP is usually an

A

increase in blood (hemorrhage), brain tissue (tumor or edema), or CSF (hydrocephalus) in the brain.
- BE THERE TO SIMPLIFY THE NEUROSURGEON’S WORDS

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55
Q

What is the best tx for increased ICP caused by a mass lesion

A

surgical removal of the mass

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56
Q

Head trauma includes an

A

alteration in consciousness, no matter how brief

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57
Q

Deaths occur at what three points in time after injury

A

Immediately after the injury
Within 2 hours after injury
3 Weeks after injury – septic infection

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58
Q

Highest risk for head injury

A

15-24 y/o
males
<5 and >75

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59
Q

Primary injury is the

A

initial damage to the brain that results from the traumatic event. This may include contusions, lacerations, and torn blood vessels due to impact, acceleration/deceleration, or foreign object penetration.

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60
Q

Secondary injury evolves

A

evolves over the ensuing hours and days after the initial injury and results from inadequate delivery of nutrients and oxygen to the cells

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61
Q

Scalp lacerations

A

easily recognized type of external head trauma
-excessive bleeding
main concern is blood loss and infection

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62
Q

Skull Fx types

A

occur with head trauma
(1) linear or depressed; (2) simple, comminuted, or compound; and
(3) closed or open

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63
Q

open fx is anything

A

exposed around the site of injury
- give antibiotics

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64
Q

Diffuse Injury

A

Concussion
Diffuse axonal injury DIA

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65
Q

Focal Injury

A

Lacerations
Contusion - bruise
Coup-Contrecoup – shaken baby syndrome

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66
Q

minor head injury GCS

A

13-15

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67
Q

moderate head injury GCS

A

9-12

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68
Q

severe head injury GCS

A

3-8

69
Q

Concussion

A

a sudden transient mechanical head injury** with disruption of neural activity and a change in the LOC
-minor diffuse

70
Q

S/S of concussion

A

brief disruption in LOC, amnesia regarding the event (retrograde amnesia), and headache
Get worst the more they get (boxers and football players with speech)
No contact sports is recommended at elementary to junior high

71
Q

DAI

A

widespread axonal damage occurring after a mild, moderate, or severe TBI. The damage occurs primarily around axons in the subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus, and brainstem

72
Q

Basilar Fx

A

base of the skull
- CSF leakage (HALO and glucose dipstick+)
- dura tear
- major infection

73
Q

Complication of Head Injury

A

Hematomas
Hemorrhages

74
Q

Epidural hematoma location

A

bleeding between the dura and inner surface of the skull

75
Q

Epidural hematoma associated with

A

neurologic emergency and is usually associated with a linear fracture crossing a major artery in the dura, causing a tear

76
Q

Acute subdural hematoma type

A

compression with increase ICP
24-48 hours

77
Q

Acute subdural hematoma s/s

A

HA
vomiting

78
Q

Epidural hematoma bleed from

A

middle meningeal artery (medical emergency)
Considered the Walking dead

79
Q

Epidural hematoma classic s/s

A

initial period of unconsciousness at the scene, with a brief lucid interval followed by a decrease in LOC
- HA, N/V

80
Q

Acute subdural hematoma bleed from

A

Venous blood – slower
**Bridging veins
- Not right away to the OR wait for them to seal on themselves

81
Q

subacute subdural hematoma

A

2nd CT notice more bleeding
- appear to enlarge over time
Tx needed
s/s increase ICP
- 2-14 days

82
Q

chronic subdural hematoma

A

Age shrinks the brain
More room in head
Without s/s and they have a bleed
Falling risk elderly
Alcoholics: multiple falling incidence bc they don’t remember the night of falling

weeks to months

83
Q

subdural hematomaoccurs from bleeding

A

between the dura mater and arachnoid layer of the meninges

84
Q

Intracerebral Hemorrhage where

A

Occurs from bleeding within the parenchyma
Usually occurs in the frontal and temporal lobes
Size and location determine patient outcome

85
Q

Subarachnoid Hemorrhage where

A

Bleeding into the subarachnoid space

86
Q

What mimics a severe migraine

A

subarachnoid hemorrhage

87
Q

Intracerebral Hemorrhage onset

A

insidious, beginning with the development of neurologic deficits followed by headache

88
Q

Intracerebral Hemorrhage mgmt

A

supportive care, control of ICP, and careful administration of fluids, electrolytes, and antihypertensive medications

89
Q

Intracerebral Hemorrhage surgical intervention

A

craniotomy or craniectomy permits removal of the blood clot and control of hemorrhage but may not be possible because of the inaccessible location of the bleeding or the lack of a clearly circumscribed area of blood that can be

90
Q

Intracerebral Hemorrhage Tx

A

Tx the s/s and wait for the blood to be reabsorbed
Diffuse axonial bleed

91
Q

Subarachnoid Hemorrhage results after

A

result of an AVM, intracranial aneurysm, trauma, or hypertension. The most common causes are a leaking aneurysm in the area of the circle of Willis and a congenital AVM of the brain

92
Q

Vasospasm

A

narrowing of the lumen of the involved cranial blood vessel

93
Q

Vasospasm monitoring

A

transcranial Doppler ultrasonography (TCD) or follow-up cerebral angiography

94
Q

Vasospasm occurs

A

3 to 14 days after initial hemorrhage, when the clot undergoes lysis (dissolution), and the chance of rebleeding is increased

95
Q

Vasospasm leads to

A

increased vascular resistance, which impedes cerebral blood flow and causes brain ischemia and infarction

96
Q

Brain Hemorrhage c/o

A

severe migraine, HA, thunderclap
photophobia, N/V
Similar to a migraine incident and need to be seen by physician to determine the difference

97
Q

Cause of Brain Hemorrhage

A

berry aneurysm in the bifurcation (trauma, uncontrol HTN)
irritates of the vessel until weakening
3-14 days after

98
Q

Tx of vasospasm

A

hypovolemic give fluids, permissively HTN, Nimotop(beta blocker/Ca blocker with regularity and on time)

99
Q

UNTx of vasospasm

A

hypoxia = ischemia= cell death

100
Q

Nursing Mgmt for Brain Hemorrhage

A

Airway - HOB 30, suctioning, O2, ABG, prevent mech vent complications
Glasgow Coma Scale score
VS - Cushing’s, T<100.4, high HR, arterial low BP
Neurologic status frequently
Presence of CSF leak

101
Q

Brain Hemorrhage major s/s

A

A,Raccoon eyes and rhinorrhea.
B,Battle’s sign (postauricular ecchymosis) with otorrhea.
C,Battle’s sign.
D,Halo or ring sign

102
Q

Rhinorrhea

A

CSF leakage from the nose
- postnasal sinus drainage

103
Q

otorrhea

A

CSF leakage from the ear

104
Q

What complications need to be assessed and prevented with CSF leakage?

A

meningitis - antibiotics

105
Q

CSF leakage determining

A

Dextrostix or Tes-Tape strip
+ glucose
HALO sign

106
Q

If the drainage is annoying, then what can the nurse do?

A

white gauze pad (4 × 4) or towel, and then observe the drainage.
- Do not pack the area of leakage – gauze under the ear to catch and collect (prevent trapping it in an infected area

107
Q

major potential complications of skull fractures

A

are intracranial infections, hematoma, and meningeal and brain tissue damage

108
Q

CSF looks like

A

straw color, sweet, sticky

109
Q

Basilar Fx should not have

A

NG Tubes – risks meningitis

110
Q

GCS range

A

3-15
< 8 intubate

111
Q

gold standard assessment tool for LOC

A

GCS

112
Q

GCS baseline is

A

the best the person can do
- when to take off sedation need HCP orders

113
Q

Nursing Acute Mgmt for head injuries

A

Maintain cerebral perfusion*
Prevent secondary cerebral ischemia*
Monitor for changes in neurologic status
Treatment of life-threatening conditions will initially take priority in nursing care*
- osmotic diuretics, SIADH, DI = electrolyte monitoring
- balance Na and glucose

114
Q

Ambulatory and Home Care for Head Injuries

A

Nutrition, Bowel / bladder control
Seizure disorders, Personality changes
Family participation and education
- increase consumption of calorie and nitrogen excretion
protein demand

115
Q

Pt Education Preventions for head Injuries

A

Advise all drivers and passengers to wear seat belts and shoulder harnesses
Caution passengers against riding in the back of pickup trucks
Promote educational programs directed toward violence and suicide prevention in the community
Teach patients steps to prevent falls, particularly in the elderly
Advise owners of firearms to keep them locked in a secure area where children cannot access them

116
Q

Head Injuries affect what cranial nerves

A

1-3

117
Q

Cranial Nerve 1 function

A

olfactory

118
Q

Cranial Nerve 1 test

A

alcohol pad

119
Q

Cranial Nerve 2 function

A

vision

120
Q

Cranial Nerve 3 function

A

most eye muscles

121
Q

Cranial Nerve 2 how to test

A

vision chart

122
Q

Cranial Nerve 3

A

follow the finger

123
Q

Types of Burns

A

Thermal
Chemical
Electrical
Smoke and inhalation
Cold thermal injury or frostbite

124
Q

Thermal burns,caused by

A

flame, flash, scald, or contact with hot objects, are the most common type of burn injury. The severity of the injury depends on the temperature of the burning agent and duration of contact time. Scald injuries can occur in the bathroom or while cooking. Flash, flame, or contact burns can occur while cooking, smoking, burning leaves in the backyard, or using gasoline or hot oil.

125
Q

Chemical burns

A

contact with acids, alkalis, and organic compounds. In addition to tissue damage, eyes can beinjured if they are splashed with the chemical. Acids are found in the home and at work and include hydrochloric, oxalic, and hydrofluoric acid. Alkali burns can be more difficult to manage than acid burns, since alkalis adhere to tissue, causing protein hydrolysis and liquefaction. Alkalis are found in cement, oven and drain cleaners, and heavy industrial cleansers.4Organic compounds, including phenols (chemical disinfectants) and petroleum products (creosote and gasoline), produce contact burns and systemic toxicity.

126
Q

Electrical burns

A

intense heat generated from an electric current. Direct damage to nerves and vessels, causing tissue anoxia and death, can also occur. The severity of the electrical injury depends on the amount of voltage, tissue resistance, current pathways, surface area in contact with the current, and length of time that the current flow was sustained Tissue densities offer various amounts of resistance to electric current. For example, fat and bone offer the most resistance, whereas nerves and blood vessels offer the least resistance. Current that passes through vital organs (e.g., brain, heart, kidneys) produces more life-threatening sequelae than that which passes through other tissues. In addition, electric sparks may ignite the patient’s clothing, causing a flash injury.
- Take path of least resistance – skin and vessels to muscle and bone

127
Q

Smoke and inhalation burns

A

noxious chemicals or hot air can cause damage to the respiratory tract. Three types of smoke and inhalation injuries can occur: metabolic asphyxiation, upper airway injury, and lower airway injury. Smoke inhalation injuries are a major predictor of mortality in burn patients. Rapid initial and ongoing assessment is critical. Airway compromise and pulmonary edema can develop over the first 12 to 48 hours.

128
Q

Superficial Partial-Thickness

A

Should heal without intervention
Superficial
Epidermal layer
Pink to red
Uncomfortable to touch

129
Q

Superficial Partial-Thickness s/s

A

Erythema, blanching on pressure, pain and mild swelling, no vesicles or blisters (although after 24 hr skin may blister and peel).

130
Q

Superficial Partial-Thickness causes

A

cause-Superficial sunburn, Quick heat flash**

131
Q

Superficial Partial-Thickness structure involved

A

Involved-Superficial epidermal damage with hyperemia. Tactile and pain sensation intact

132
Q

Deep Partial-Thickness

A

Epidermal and dermal layer involved
Red mottled pink edges, hair remains intact
Very painful
Takes 2-4 weeks to heal

Sensitive to touch, cold and warm air
Moderate to severe pain
Blisters

133
Q

Deep Partial-Thickness skin destruction

A

Fluid-filled vesicles that are red, shiny, wet (if vesicles have ruptured). Severe pain caused by nerve injury. Mild to moderate edema.

134
Q

Deep Partial-Thickness causes

A

Flame
Flash
Scald
Contact burns
Chemicals
Tar, cement
Electric current

135
Q

Deep Partial-Thickness structures involved

A

Epidermis and dermis involved to varying depths. Skin elements, from which epithelial regeneration occurs, remain viable.

136
Q

Full-Thickness Burns

A

Full dermal layer involved
White, dry, leather like texture
No nerve endings = no pain

137
Q

Full-Thickness Burns skin destruction

A

Dry, waxy white, leathery, or hard skin. Visible thrombosed vessels. Insensitivity to pain because of nerve destruction. Possible involvement of muscles, tendons, and bones

138
Q

Full-Thickness Burns cause

A

Flame
Scald
Chemical
Tar, cement
Electric current

139
Q

Full-Thickness Burns structure involved

A

All skin elements and local nerve endings destroyed. Coagulation necrosis present. Surgical intervention required for healing

140
Q

ED, burn arms with grease fire
Indicated, Nonessential, contraindication

A

Indicated – Ivs, analgesics, tetanus toxoid
Nonessential – O2, EKG,
Contraindicated – shower in the first 12 hours

141
Q

Burn from chest up
Indicated, contractions

A

Indicated O2, 2 IVS, analgesics, possible intubation
Contra – cool room

142
Q

Inhalation Injury s/s

A

Blisters, edema
Difficulty swallowing
Hoarseness
Stridor
Retractions
Total airway obstruction
Damage mucosa
soot

143
Q

Metabolic Asphyxiation

A

primarily carbon monoxide (CO) or hydrogen cyanide. Oxygen delivery to or consumption by tissues is impaired. The result is hypoxia and, ultimately, death whencarboxyhemoglobin(i.e., hemoglobin combined with CO) blood levels are greater than 20%. CO and hydrogen cyanide poisoning may occur in the absence of burn injury to the skin.

144
Q

Upper airway injury

A

swelling can be massive and the onset rapid. Flame burns to the neck and chest may make breathing more difficult because of the burn eschar, which becomes tight and constricting from the underlying edema. Swelling from scald burns to the face and neck can also be lethal, as can external pressure from edema pressing on the airway. Mechanical obstruction can occur quickly, presenting a true airway emergency.

145
Q

Lower airway injury pulmonary edema occurs after

A

12-48 hours after the burn - ARDS

146
Q

Do you wait for intubation with inhalation injuries?

A

no
Do not wait for intubation due to swelling
Burnt skin and mucosa become tight and lead to mechanical obstruction

147
Q

Electrical Injury

A

Masked marauder – under the skin is a tunneling mess going through everything from path of least resistance but only appears as a tiny hole

  • EKG for dysrhythmias, SEVERE METABOLIC ACIDOSIS, AND MYOGLOBINURIA
148
Q

How to tell the extent and depth of burn injuries?

A

Rule of Nines, Lund-Browder, or the Berkow charts calculate the total body surface area (TBSA) burned
The Rule of Palms can be used for scattered burns

149
Q

Explain the Rule of 9s

A

Head front = 4.5%
Head Back = 4.5%
Upper chest and lower chest
and same with the back = 9% each
each leg as a whole is 18%
each arm is 9%

150
Q

Palmar Method explaned

A

The pt palm is 1%
-scattered burns

151
Q

Referral Criteria for burn victims

A

1.Partial-thickness burns >10% of total body surface area (TBSA)
2.Burns that involve the face, hands, feet, genitalia, perineum, or major joints**
3.Third-degree burns in any age group**
4.Electrical burns, including lightning injury**
5.Chemical burns**
6.Inhalation injury**
7.Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality risk (e.g., heart or kidney disease, diabetes)
8.Any patients with burns and concomitant trauma (e.g., fractures) in which the burn injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn center. The HCP will need to use his or her judgment, in consultation with the regional medical control plan and triage protocols.
9.Burn injury in children in hospitals without qualified personnel or equipment needed to care for them
10.Burn injury in patients who will require special social, emotional, or long-term rehabilitative intervention

152
Q

Associated Trauma for Burn victims

A

Remember the ABCs of trauma
Burns and inhalation injury frequently mask other injuries
Fractures
Spinal cord injury
Other trauma
- fluid and electrolytes shift
- inflammation and healing
- immunity

153
Q

Fluid and Electrolyte Patho for burns

A

Fluid and Electrolyte shift
Inflammation and Healing
Immunologic Changes
Decrease vascular volume – cap becomes permeable (interstitial)
Decreased cardiac output
Increase blood viscosity

154
Q

Inflammation and Healing patho for burns

A

Burn injury to tissues and vessels causes coagulation necrosis. Neutrophils and monocytes accumulate at the site of injury. Fibroblasts and newly formed collagen fibrils appear and begin wound repair within the first 6to 12 hours after injury

155
Q

immunity patho for burns

A

skin barrier to invading organisms is destroyed, bone marrow depression occurs, and circulating levels of immunoglobulins are decreased. Defects occur in the function of white blood cells (WBCs). The inflammatory cytokine cascade, triggered by tissue damage, impairs the function of lymphocytes, monocytes, and neutrophils. Thus the patient is at a greater risk for infection.

156
Q

S/S of electrolyte and fluids

A

Na INSIDE THE CELL
K outside the cell
Albumin, Na and water into interstitial space

157
Q

Emergent Phase mgmt

A

care mainly focuses on airway mgmt
fluid therapy - 2 IVlarge
wound care
emotional support for all
teaching

Protect the team before providing care
ABCs of trauma
Protect the airway
Fluid needs
Metabolic and electrolytes
Psychosocial needs of the patient and the staff

158
Q

What burn victim is the first to be seen?

A

deep partial thickness
- prepare for intubation
- post-anesthesia
- full thickness with dressing change

159
Q

What is the 1st thing needed in assessing a burn victim?

A

protect environment

160
Q

Fluid Resuscitation for Burn Victims for the first 24 hours

A

[Weight in Kg] X [TBSA burned] X [4 mL]
divide by half = 1st 8 hours
divide by half that number = next 8-8 hours

double check in L

161
Q

Using the Parkland formula, the nurse determines that a patient requires a total of 12 L of fluid in the first 24 hours post injury. How much of the total volume needs to be given within the first 8 hours?
A. 4,000 mL lactated Ringer’s
B. 6,000 mL lactated Ringer’s
C. 8,000 mL lactated Ringer’s
D. 10,000 mL lactated Ringer’s

A

B. 6,000 mL lactated Ringer’s

162
Q

Fluid losses in burn victims

A

3rd spacing
blisters and exudates
edema
insensible loss 30-50mL/hr

163
Q

Fluid Mgmt after first 8 hours

A

Light wt diuretic
Turn down fluid given
Fluid loss from breathing 30-50 mL
Intubation
Humdify warm air
Blister formation =fluid loss

164
Q

Reparative Phase

A

Wound care
Nutritional support
Management of pain
Prevention of contractures
Wound management
Psychosocial issues
Use of topical antimicrobials
Early debridement
Early excision and grafting
Contractions = passive or active ROM with analgesics
Scrubbed with brush - debridement
Strict infection control practices (i.e., physical isolation in a private room, use of gowns and gloves during patient contact, and handwashing before and after each patient visit
Psych consult and antidepressants

165
Q

Rehabilitation and Reconstruction Phase of Burn victims

A

On going skin needs
Activity needs
Self-concept and depression
Noncompliance with care

166
Q

Rehabilitation and Reconstruction Phase occurs

A

7-8 months after

167
Q

Reconstruction Phase goals

A

(1) work toward resuming a functional role in society and (2) rehabilitate from any functional and cosmetic postburn reconstructive surgery that may be necessary

168
Q

Mature healing is reached in about

A

12 months when suppleness has returned, and the pink or red color has faded to a slightly lighter hue than the surrounding unburned tissue.

169
Q

A patient who is admitted to a burn unit is hypovolemic. A new nurse asks an experienced nurse about the patient’s condition. Which response if made by the experienced nurse is most appropriate?
“Blood loss from burned tissue is the most likely cause of hypovolemia.”
“Third spacing of fluid into fluid-filled vesicles is usually the cause of hypovolemia.”
“The usual cause of hypovolemia is evaporation of fluid from denuded body surfaces.”
“Increased capillary permeability causes fluid shifts out of blood vessels and results in hypovolemia.”

A

“Increased capillary permeability causes fluid shifts out of blood vessels and results in hypovolemia.”
????????? - doule check

Module 7 (Critical Care) (22 decks)

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