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Trauma > Critical care and burns > Flashcards

Critical care and burns Flashcards

1
Q

Trauma associated deaths - What are causes of the first peak, second peak, third peak and later peak injuries

A

1) first peak - detrimental and non-survivable injuries, catastrophic haemorragic injuries such as aorta trisection
2) second peak - bleeding injuries that are life-threatening that requires intervention quickly such as haemopneumothorax
3) third peak - sepsis, MOFS, infection - most common cause of late trauma deaths
4) later peaks - mostly self-infliceted deaths caused by suicides

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2
Q

Differences between conflict, austere, and far from help care

A

Far from help - simply being far away from help
austere - strict, simple environment whereby care MAY be difficult to access
conflict - not austere operating environment
Expertise! training, competence and currency - capacity to operate on speciliased surgery is esp. limited in war

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3
Q

How does austere and conflict care differ?

A

Improvisation, types of injuries, surgical approach and environment (e.g. safety)

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4
Q

What to consider in conflict conditions (how it differs from normal hospital care)

A

Limited resources
Collaboration/cooperation with other governmental organisations
Hostile/unsafe environment

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5
Q

Unique patterns of injury in war

A

survival > aesthetics - massive amputations etc.
sexual violences - fitsulae, genital mutilation
Extreme age - mainly young children and very elderly who can’t or refused to evacuate

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6
Q

Principle of governance

A 
Humanity 
Neutrality 
Impartiality
Independence 
"Neutral human beings
 should be Impartial and independent"
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7
Q

Are military forces completely neutral?

A

No, not completely. They are NOT operational dependent

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8
Q

Primium non nocere

A

First do no harm

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9
Q

3 Principle of burns management and dressings

A

COVER - prevent fluid loss and infection
REDUCE SCARRING - restore characteristics of injury area (colour, contour and texture)
INDEPENDENCE - allow movement and functional recovery

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10
Q

4Ps of treating burns patients

A

Pain - analgesia prior to treatment (internasal diamorph), if >10%TBSA ketamine shower
Prevent - infection prevention, clean wounds with chlohexidine or soap and water, prophylactic antibiotics only if sever or have clinical signs (Flucloxacillin G+; gentamycin G-)
Psychology - both patients and family, mostly family during acute phase
Position - oedema control, movement to prevent shortening of tendons and for functional maintenance/recovery

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11
Q

Principle of burn wound management (ABCDD)

A

A - analgesia - prior to any procedure, ket. shower if >10%
B - Bed preperation for wounds - deroof blisters, necrotic fibrinous tissues etc.
C- clean wounds with anti-microbials solution (e.g. chlohexidine)
D - depth of burns assessement
D- dressing to cover (aseptic if possible)

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12
Q

Which protocol comes first in burns trauma? to treat burn or trauma first?

A

ATLS comes first - C-ABCDE approach, don’t be distracted by burns. Following this then treat burns - ABCDD, give fluid resuscitation as appropriate (TBSA% > 10 &15% for children and adults, respec)

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13
Q

Fluid resus protocol for paeds and adult burns

A

Day1 - parkland formula using hartmann solution
-TBSA> 10% (paed);15%(adult). 4mL/Kg/%TBSA, 50% first 8 hours, 25% subsequent 8%, 25% last 8 hours
- paeds require maintenance fluid at hourly rate due to tendency to hypoglycaemia - first 10kg (4mL/kg) + next 10kg (2mL/kg) + >20kg (1mL/kg) of 0.9%saline+5% dextrose
Day 2 - basal + evaporative loss
- Basal - 1500mL per body surface area (BSA) per day
- evap - (25 or 35 + TBSA) x BSA = mL/hr

Increase bolus if: inhalation injury, full thickness, delayed resucitation, electrical/chemical burn, alcohol toxication, associated trauma

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14
Q

Principle of good wound dressing

A 
Prevent infection 
Prevent fluid loss
Warm moist environment for wound healing and to prevent spreading of wound (NB. NO COTTON, too moist and bed for microbe breading)
Allow movement 
Non-traumatic
Oedema control
Reduce scarring 
Cost-effective
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15
Q

Areas of special care in burns

A

Face (eyes, ears)
Hands, fingers - not boxing style wrapping
Perineal and genital burns

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16
Q

Common dressings

A

Jelonet/Bactigras - holding dressing, daily
Urgotul Ag - 3-5 d ay change
Acticoat - partial thickness, post-OP, expensive
Meplilex Ag - not for clincally infected wounds, 3-5 day change
Flamazine - ointment, cost-effective, leukopenia if longterm, partial and deep dermal, use after depth assessemnt
Flammacerium - conservative approach, form eschar, deep dermal, full thickness
Diphoterine (chemical burns)

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17
Q

Typical burns dressing consist of

A

Non-adherent layer
Absorbant layer
Bandage

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18
Q

Definition of sepsis

A

Life-threatening condition that arise when the body’s respones to an infeection damages its own tissue and organs

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19
Q

Peak incidence of sepsis

A

~12 days (at week 2)

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20
Q

Incidence of MODS in acutely ill patients

A

~50%

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21
Q

MOFs is the most common cause of late trauma death

A

yes

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22
Q

Pathogenesis of sepsis

A 
Tissue injury (trauma) activates immune response (inflammatory mediators). 
Infection exacerbates this response.
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23
Q

SIRS criteria

A

SIRS is sterile

  • RR>20
  • HR>90
  • Temp <36, >38C
  • WBC<4K, >12K or banded NPs>10%
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24
Q

Can infection exist without SIRS

A

YES

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25
Q

def. sepsis Dx clinical criteria

A

SIRS + SUSPECTED OR CONFIRMED INFECTION (blood culture)

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26
Q

Severe sepsis clinical Dx criteria

A

Circulatory — SBP<90 or MAP <65 or reduction in SBP > 40 mmHg from baseline
Respiratory — SpO2 < 90% or PaO2:FiO2 < 40kPa
Renal — UO <0.5/kg/hr for >2hr or creatinine >176umol/L acutely
Haematological — platelets < 100 x109or INR > 1.5 or APTT > 60s
Hepatic — Plasma lactate > 4mmol/L or bilirubin >34umol/L
“Brain” — acute alteration in mental status

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27
Q

septic shock

A 
Circulatory failure (acute) unexplained by other causes 
- persistent hypotension (MAP<65; or reduction in SBP by 40mmHg from baseline) despite adequate volume resus
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28
Q

Sepsis 6

A 
Monitor UO 
Bloods 
Fluids 
Lactate 
O2 
Broadspec antibiotics
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29
Q

Delay in sepsis care increase mortality by X%?

A

delay every hour increase mortality by 7.6%

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30
Q

cfDNA and citH3 in early trauma

A

high cfDNA and citH3 within first hour but decrease later on

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31
Q

Actin role in sepsis/NETS

A

Excessive NETS and poor scavenging/breakdown of NETS thought to activate immune response, leading to SIRS.
Actin scavenger system seemed impaired (actin inhibits Dnase1 activity that normally breaks down NETS).

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32
Q

Whats the bad side of having scars

A

scars over joints can lead to movement issues esp. if these scars contract

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33
Q

current treatment in burns

A

(meshed) Skin graft, dressing, skin substitute, skin replacement (xenografts, cadaver), stem cell therapy (spray)

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34
Q

Sequences of physiological events after traumatic (burn) injury

A

Tissue damage
Inflammation
tissue remodelling
Scar tissue formation

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35
Q

Challenges associated with burn injury

A

Infection
Pain
Scarring/aesthetics -lead to mental problem

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36
Q

Why do we generate scars

A
  • Scarring due to failure in regeneration

- Regeneration failed due to scarring

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37
Q

Problems associated with scarring

A

Movement problems

Permanent, temporary discolouration

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38
Q

which cell type is the first to be obliterated injury

A

melanocytes - lead to discolouration

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39
Q

Types of scars and fibrosis

A 
Normal 
Hypertrophic
Keloid 
Contractures
Adhesions
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40
Q

Scar reduction therapies

A

Messages
Water jets (hydrotherapy)
Dermal roller

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41
Q

How does scar reduction therapy work?

A

We don’t really know, suppose mechanistically messaging the skin activates cells and promote production of collagenase which breaks down collagen

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42
Q

comparison of a good and bad scar

A

Good scar: good weaving of collagen matrix. Melanocyte present, retain dermal ridges, high elastin content.

Bad scar: parellel, flat arrangement of collagen fibres. Flat dermal ridges, little to no melanocytes and elastin

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43
Q

Mature scar characteristics

A

Little mature collagen present, may have prolonged collagen production phase and inappropriate amount of collagen. Collagen I:III = 90%:10%.

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44
Q

X% of protein in scar is collagen

A

50% collagen

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45
Q

Poor scar consist of

A

low elastin + inappropriate collagen deposition - increase rigidity

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46
Q

Age effect on skin

A

Smoothing of ridges
Thinning of skin due to atrophy of layers
Reduced stem cell capacity
Incrase AGE deposition (lipofuscin) - can interfere with cellular process and make cells more stressed, rendering them senescent
Disorganisation of collagen fibres
Reduced vasculature
Reduced enzyme secretion

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47
Q

Fibrocytes/pericytes charcateristics

A

Blood-borne cell type with FB-like properties.
Believed to be precursors of FB.
Plays an active role in wound healing
Distinct cell phenotype

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48
Q

Current innovative therapy in burns

A 
SC spray (e.g. keratinocyte spray, stem cell spray)
Regenerative soft tissue sponge
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49
Q

Mechanism of scar formation

A

Timeline to scaring normally a year but can take as long as required. Good healers has shorter inflammatory phase.

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50
Q

3 phases of scar formation

A

Inflammatory
Proliferative
ECM deposition and remodelling phase

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51
Q

Aim for scar-free regeneration follow burns and trauma

A

Studying the 3 phases in good and bad healers. Attempt to recapitulate baby healing phase (<18months). Normally each phases are shorter, in particular the inflammatory phase

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52
Q

Contracture of scars caused by

A

Myofibroblasts arising 1-2 week post-injury by the promotion of TGFb and PDGF

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53
Q

Inappropriate presence of myofibroblast can result in?

A

Contraction of scars forming contractures. Can lead to movement problems if bridges joints.

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54
Q

Inx of burns admissions in ED, hospital and those requiring resus? (per year)

A

130000 (ED)
13000 (hospital; 10%)
1300 (resus; 1%)

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55
Q

Most common type of burns in adults and paediatric

A

Adults
- flame (60%), scalds (30%), contact (15%), chemical (10%), electrical, radiation and friction

Paeds
- scalds (40-60%), flames (20%), contact (1-%), chemical (2%), electriacal radiation (1%, esp. summer), and friction

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56
Q

Where do burns occur?

A 
mostly home (kitchen, bathroom) ~60%
Workplace
Road, outdoors etc
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57
Q

Why is Lund and browder chart the best way to assess TBSA?

A

CHILDREN HEAD:TORSO ratio is greater

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58
Q

Function of the skin

A 
Immunological (surveillence) 
physical and chemical barrier 
sensation 
aesthetics 
metabolic (e.g. temp, fluid regulation, vit D synthesis) etc.
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59
Q

Blood supply in the skin layer

A

mainly restricted to the dermis

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60
Q

Describe the jackson model of burns

A

A 3D model proposed to describe what occurs following burn injury.
Zone of necrosis/coagulation - necrotic tissue where burns first occur (usually zone of first contact)
zone of stasis - 50% of cells are necrotising, salvagable zone and the aim of resus is to salvage this zone. appropriate treatment prevent spreading of the wound
Zone of hyperaemia - inflammatory reaction/response to trauma, can turn into zone of stasis w/o appropriate Mx

61
Q

Cascade of Mx of burns from prehospital care to hospital

A

1) ABCDE
2) Rapid transport to hospital + Hx prior to intubation (non-accidental/self-inflicted)
- always suspect inhalation injuries
3) ABCDD + resus if TBSA >10/15%

62
Q

Catheterise bladder if burns >X TBSA%?

A

25%

63
Q

Resus endpoint

A

UO 0.5-1mL/kg/hr (adult); 1-2mL/kg/hr (paeds, inhalation)
RR<20, HR <120
MAP >60mmHg
Base excess improved (E.g. better lactate etc)

64
Q

CoHb % and its outcomes

A

> 50% lethal, coma
40% collapse
30% dizziness, reduced vision
10-20% headache

65
Q

Usual Tx for CO poisoning

A

High flow O2 untill O2 molecules replace those of CO, oxygen sats may not be accurate

66
Q

CN characteristics, halflife and antedote

A

CN arise from house fires (e.g. burning of furniture)
Odorless and commonly forgotten
Pts may be present with ribina-like fluids
T1/2 = ~3hrs
IF suspect - give antedote
Antedote - hydroxycarbalamine 75ugm/kg

67
Q

Why do we need fluids for burns patients?

A

Burns causes capillary damage, leading to extravasation of plasma protein, altering the oncotic pressure, thereby leading to acute fluid shifts/fluid loss.
Loss of fluids can worsen burn wounds in depth and in size.
Haemoconcentration can increase risk of thrombosis and organ failure.
Hypovolaemia can lead to cellular shock (persistent shock

68
Q

Over-fluid resuscitation leads to what in the brain, lung, gut, kidney, other tissues and systematically?

A 
brain - cerebral oedema 
lungs - ARDS
Gut - malabsoption, shedding of EGL
kidney - ceasation of filtration, anuric, inability to filtre toxins 
tissue oedema
compartment sydrome, MOFs
69
Q

Under-fluid resus can lead to

A

thrombosis (haemoconcentration), increase likelihood of immune cell captivation (slow flow), hypoperfusion and MOF

70
Q

High Na+ as a result of continuous saline administration can lead to?

A

Hypernatraemia + hyperchloraemia leading to alkalosis.
High Na+ can enter cell and change osmotic pressure, resulting in cell death (burst) and bind to collagen resulting in breakdown of collagen

71
Q

Under what situations should extra bolus of fluid be given in addition to the primary resus protocol?

A 
extra bolus of fluids should be given at an hourly rate if: 
inhalation injry 
full thickness burns
delayed resuscitation 
Alcohol intoxication 
assocaited trauma
electrical injuries (high voltages)
72
Q

Fluid resuciation endpoint

A

UO = 0.5-1.0-2 mL/hr/kg
MAP > 60mmHg if patient not diabetic, not on diuretics, or intoxicated + concentrated urine
Improved base excess – e.g. lactate, HCT
Monitor CVP but do not treat CVP, treat MAP changes instead

73
Q

when was the parkland formula devised? and by whom?

A

1968, baxter

74
Q

1842 coconut grove fire (cope and moore) found out 4 important concepts which were

A

1) oedema can be generalised and localised
2) plasma is lost into third space
3) devise first fluid resus formula for the first 8 hours
4) correlated fluid loss to weight

75
Q

What methods do we use to tackle trauma

A 
Phaemaceuticals (most common)
Tissue engineering (e.g. implants)
Biomaterials (e.g. to deliver a therapeutic)
76
Q

define tissue engineering and biomaterials

A

Tissue engineering - develop tissue and organs to provide scaffold; i.e. things to impregnate cells with

Biomaterials - any type of materials that help with biological functions (e.g. wooden leg, hydrogels)

77
Q

Challenge in tissue engineering

A

The multiplex structure in human is difficult to replicate and engineer

78
Q

Fabricating microstructures tend to take bottom-up or top-down approach?

A

Bottom-up approach

79
Q

examples of biological colloidals

A

blood, bone, cell membrane, vesicle, milk

80
Q

define colloid chemistry

A

essentially suspensions, mixing two media that does not mix together

81
Q

Role of TGFb1 in trauma and scars

A

TGFb1 drive FB into MFB which produce extracellular matrix. MFB is also responsible for contractures if they persist after re-epithelialisation

82
Q

If healing occurs in first two weeks can we avoid scar formation ?

A

yes

83
Q

Anti-scarring hypothesis of decorin

A

decorin decorate collagen fibrils to help arrange F-collagen scaffold

84
Q

Describe the reconstructive ladder from the early to late stages

A

Secondry intention, primary intention (delayed primary closure), NPWT, skin graft, skin substitute, tissue expansion, local flaps, regional flaps, distal flaps, free flaps, pedical flaps, spare parts, regeneration

85
Q

What is a split skin graft and how does it differ from a full thickness skin graft?

A

Split - epi + part of dermis

full skin graft - epi + full dermis

86
Q

Give example of direct closure

A

Rarely performed early - often delayed

Amputation stump, commonly NPWT is used as well

87
Q

What is NPWT and the advantages of using it

A

negative pressure wing therapy, vaccum system placed on wound to suck out exudate.
Promote wound healing (excess fluids can impede cell growth/proliferation), promote cell division and granulation tissue formation
Decrease local swelling, improve ciruclation to wound bed
Reduce bacteria growth**

88
Q

What are the three prinicples for successful skin grafting

A

Tolerance to ischaemia
Metabolic activity of the graft
Vascularity of the donor site

89
Q

The 4 phases of skin grafting

A

1) Fibrin adhesion - skin graft is “stuck” onto the wound with the help of exudate and fibrin (ischaemic)
2) plasmatic imbibition
3) revascularisation - skin graft will live on exudate and gradually anastomosis occurs which connects graft and host vessels.
4) remodelling - revascularisation

90
Q

What is the problem of local flaps?

A

zone of injury problems

91
Q

Improved survival on battlefield injuries due to the use of

A 
body armour 
field aplied tourniquets
homeostatic agents (chitin)
Early Dx/Tx of shock -- transfusion of 1:1:1 PLT:RBC:FFP
early intensive prehos treatment
92
Q

Timing of reconstruction

A 
Clean, non-contaminated wound
Adequate debridement 
stablise bones and rigid fixation of fratures - orthopedics first 
Rehab early 
Early soft tissue closure
93
Q

Obstacles in reconstructive surgery

A

Contamination - bacteiral, unusual organism (fungal)
mutiple concurrent injuries + multiple regions
Limited donor sites
CAtabolic phnoetype
Difficult to get out of zone of injury for safe flap repair
difficult to achieve non-contaminated wound bed

94
Q

Advantages of tissue engineering

A

patients own cells so it shoudnt be rejected

reduce need for donor organs

95
Q

Describe the bottle up approach

A

chemistry based apprach - try to grow particles. depends on self-assembly phenomenon

96
Q

Nuclei production usually through what methods

A

supersaturation, precipitation

97
Q

Scar formation and its timeline

day 7, 7-14, 14-21, 21-30, >30 days

A 
<7 days - no scarring 
7-14days - 13% 
14-21 days - 35% 
21-30% - 86%
>30 days - 98%
98
Q

Strategies to enhance wound closure

A 
Delivery of pharmaceuticals - most comon
deposit cells (keratinocytes; stem cells) to acclerate re-epitherliasation
99
Q

Anti-scarring hypothesis

A

Provide microenvironment whereby anti-scarrying protein can control the healing the process via

  • sequestering GF
  • aligning the collagen
100
Q

Challenges in designing materials for dynamic regions of the body

A 
Small volumes 
Contours and changing topologies 
Difficulties in recapitulating all the complex layers in skin (components in tissue)
body movement 
Mechanical manipulation 
Natural replacement of local fluids
101
Q

Does decorin work?

A

Decorin work as a scaffold for collagen matrix to form accordingly to its natural arrangement
Re-epithelialisation increased from 12-24% 3 days post-wounding
No systemic exposure

102
Q

Use of fluid gels

A

Ocular bandage - enhance architecture of cornea

Joint lubrication - e.g. OA

103
Q

GOAL OF PRIMARY SURVEY

A

Identify life-threatening conditions and intervene immediately

104
Q

Primary survey assessment in ICU

A 
C-ABCDE 
A - airway w/ C-spine control, suspect inhalation injury, CO/CN poisoning through exam and Hx 
External bleed
Carotid pulse
Central cyanosis
Auscultation
Shock, CRF, temp  
EJV/ conjesion 
Pupil, conjunctivae filling
If in doubt intubate
105
Q

Oedema max at

A

12-36 hrs

106
Q

ICU scanning

A 
Whole body CT 
USS
MRI
Operation
X-Ray 
eFAST
107
Q

Goal in ICU

A

Resuscitation + restore physiological function and perfusion
Complete Hx/Dx
Schedule required Tx/Mx
Early physio and rehab

108
Q

Shock resus goal and monitor

A

Goal to restore tissue perfusion
Monitor
- Metabolic - acidosis - lactate, breathing
- Circulatory - periphery pulse, ScvO2, Peripheral perfusion
UO

109
Q

When to perform fluid challange and how

A

Hypovolaemia in pts requiring correcting.
Give 500mL of crystaloids <15 mins, position in supine pos. with leg raise at 45 degrees. check JVF and SV. Responsive = Preload and SV increase. Unresponsive = increase preload with little or no SV raise.
JVF fill can indicate congestion

110
Q

Oesophageal doppler is used for

A

monitoring decending aorta blood flow velocity

111
Q

Abdominal injury in ICU - IAP at 15mmHg and 20mmHg are indicated for

A

IAP 15 - venous congestion, organ dysfunction

IAP >20 - surgical decompression necessary to prevent compartment syndrome

112
Q

Role of TGFb1 in scarring

A

TGFb pathway in FB seemed to be asscoiated with scarring. Decorin inhibits this pathway

113
Q

What is decorin

A

ECM Glycoprotein that inhibits TGFb pathway, achieving anti-fibrotic properties. Binds to collagen and assist arrangement of F-fibrils

114
Q

examples of acute phase proteins that decreases during truama

A

transferrin
alpha-anti-trypsin
prealbumin
Albumin

115
Q

function of CRP

A

opsonisation, inhibit platelet aggregation, neutralise NETs

116
Q

Percentage of NP is

A

50-60%

117
Q

which of the following is NOT an acute phase protein involved in wound healing?

a) Collagen.
b) Fibrinogen.
c) Fibronectin.
d) Haptoglobin.

A 
A- Collagen.
B- Fibrinogen.
C- Fibronectin.
D- Haptoglobin.
Answer: A
118
Q

Name 4 proinflammatory MEDIATORS released during acute inflammation (see pathophysiology lecture)

A 
PGE2/PGI2
LTB4
VEGF 
BRADYKININ
HISTAMINE
THROMBIN...
119
Q

zones of burns injury

A

zone of coagulation/necrosis
Zone of stasis
Zone of hyperaemia

120
Q

Trauma account for X% of death worldwide. Haemorrhage account for Y% of trauma deaths. 1/4 patients are present with what condition which contribute to this?

A

10% of death worldwide
40% deaths due to haemorrhage
1/4 patients have idiopathic coagulopathy. Also use of warfarin, clopidegril and aspirin can contribute to this

121
Q

Coagulopathy of trauma is due to

A

Hyperfibrinolysis
- tPA released by EC overwhelm PAI-1, leading to plasmin activation and therefore prevent clot formation.
acidosis, hypothermia can also affect platelet reactivity

122
Q

NETS and histones are ( ) charged. Which one forms a procoagulant surface

A

NETs -
histone +

NETs act as procoagulant surface promoting thrombus formation. but both are potent immune stimulators

123
Q

Lactate (mmol/L) and mortality after trauma resus

A

<1 18%
2-4 74% (nb. severe sepsis lactate > 4mmol)
>5 100%

124
Q

Failure of substrate delivery due to poor perfusion can lead to

A
  • cellular shock - exacerbate infalmmatory conditions under hypoxia
  • blood loss
  • pump failure
  • failure of microvascularture (ischaemia/reperfusion)
125
Q

Production of acute phase protein is induced by (IL-?)

A

IL6.

proinflammatory cytokines released act on innate cells such as MP, which in turn secrete IL-6 to stimulate liver to produce acute phase proteins

126
Q

Examples of acute phase proteins

A 
CRP
haptoglobin - binds free Hb
Fibrinogen 
Fibronectin 
Alpha 1 anti-trypsin 
alpha 1 anti-glycoprotein
127
Q

Endocrine response to trauma is charactersied by

A

increase in stress hormones - vasocontriction/water/Na+ retention
- cortisone/cortisol
- aldosterone
- ADH (thirst)
Reduce DHEA (shift towards stress hormones production)
ANP (atrial natruietic peptide) - normally decrese renin/prmote vasodilation

128
Q

Challenges associated of burns injury

-IPSA

A

Infection
Pain
Scarring
Aesthetics

129
Q

Scarring can lead to what problems

A

Discolouration of skin
Movement if bridged joints
Disfiguration (e.g. keloids)
All of which contributes to physical and psychological consequences

130
Q

Scar formation phases (4*) and describe what occurs during then

A

1) haemostatic phase - stop bleeding, coagulation take place
2) inflammatory phase - tissue injury attracts NPs (acute), MPs and later lymphocytes to fight against infections, clear debris and promote wound healing
3) Proliferative phase - migration and proliferation of fibroblasts to the site of injury. Re-epithelisation occurs. Formation of tissue granulation
4) ECM remodelling. Deposition of ECM andsecretion of proteolytic enzymes to reorganise collagen structure. Scar formation and maturation

131
Q

Goal of scar free healing is to

A

Recapitulate the phases seen in scarfree healing in babies <18 months.
through secretion of GF and alignment of collagen.

132
Q

Biomarkers of scarring

A

Connexin
Cortactin
Elastin
Integrin

133
Q

What cells are responsible for pigmentation in the scar and what enzyme within it

A

melanocytes

tyrosinase

134
Q

Systemic changes in major burns in the CVS, RS, metabolism and immune system

A

CVS - REDUCED myocardial contractivity, increase vessel permeability, vasoconstriction of the splenic and peripheral systems

RS - ARDS, bronchoconstriction
Metabolic - increased BMR by 3-fold. For a 40% TBSA, BMR can increase up to 200%

Immune system - immunosuppressed state

135
Q

Pathophysiology of burns

A

Burns leads to release of inflammatory mediators and changes in the microvascularture.

Microvasculature changes include: increase vascular permeability and extravasation of plasma protein leading to acute fluid shift. Exacerbated by the release of inflammatory cytokines.

This leads to peripheral oedema and reduced intravascular volume, leading to hypovolaemia shock. Cellulra shock can take place as a result of hypovolaemic shock. Altogether causing burn shock

136
Q

Damage mechanism associated with heat burns and chemical/electrical burns

A

Heat burns - protein denaturation, coagulative necrosis

chemical and electrical - distruption of/ damage to membrane integrity

137
Q

What to be aware of during Airway assessment in burns

A

Hx of incident - self-inflicted? non-accidental? Fire? Suspect inhalation and CO/CN poisoning
Dentures
ET tube - size, length, type, fixation (crown, nasal)
NEVER CUT TUBE

138
Q

Suspect cyanaide poisoning when

A

metabolic acidosis (high lactate anion gap)
Hypotension, bradycardia and pulmonary oedema.
Smell of almonds
NB Incident Hx important

139
Q

What needs to be noted for a Burn assessment

A 
TBSA (size)
depth
site of injury 
Associated injuries
inhalation injury
Age, Medical HX
140
Q

Def. of MOFs

A

Altered organ funtion in acutely ill pts requireing intevention ro achieve homeostasis

141
Q

In cohorts of adult ICU trauma patients, a MODS incidence of ______% has been reported

A

47-56%

142
Q

Most common cause of late trauma deathis

A

MOD

20-75% mortality in patients having at least two-organ failure

143
Q

Long-term functional status affected by the development of MODS; ____ times increased risk of requiring personal assistance in daily living for those patients who developed MODS

A

4x

144
Q

pathological scarring incidence in burns, surgical wounds and keloids

A

burns ~65%
surgery ~35%
keloid 6-16%

145
Q

How do we control colloids

A

through chemical and physical barriers

146
Q

Healing and scar formation

A

Scarring occurs when the balance between the two stages is lost, resulting in an uncontrolled deposition of ECM and change in collagen microstructure (alignment )

147
Q

Uncontrolled deposition of ECM leads to change in collagen alignment eventually lead to scar development

A

yes

148
Q

Use of fluid gels

A

ocular bandage
OA - lubrication of joints
Bandages in cartilage defects

Trauma (5 decks)

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