CASE 10 - BURNS Flashcards
1
Q
Which layers of the skin are vascularised?
A
Dermis and hypodermis
2
Q
In which layer of the skin are adipocytes located?
A
Hypodermis (subcutaneous layer)
3
Q
What are the differences between thick and thin skin? (Location, histology, thickness)
A
THICK skin is located on the palms and soles of the hands and feet, contains 5 different layers, and the epidermis is about 5mm thick.
NO sweat glands or hair follicles. YES sebaceous glands.
THIN skin is located everywhere else on the body, contains 4 different layers (lacking a stratum lucidum), and the epidermis is ~0.1mm thick.
YES sweat glands, hair follicles, and sebaceous glands.
4
Q
Name the 5 TYPES of cells in the epidermis
A
- Stem cells (located in stratum basal)
- Keratinocytes
- Dendritic/Langerhans cells
- Merckel/tactile cells
- Melanocytes (also in stratum basale)
look @ a diagram
5
Q
What is the function of the STEM cells within the epidermis?
A
Undifferentiated cells that give rise to keratin, which comprise the majority of the epidermis
6
Q
What is the function of the KERATINOCYTES within the epidermis?
A
Synthesise keratin (which offers protection and acts as a moisture barrier)
7
Q
What is the function of the MERCKEL/TACTILE cells within the epidermis?
A
Touch receptor cells
Prominent in areas such as the lips and oral cavity
8
Q
What is the function of the DENDRITIC/LANGERHANS cells within the epidermis?
A
Present pathogens (that have penetrated through the epidermis) to the immune system
9
Q
What is the function of the MELANOCYTES within the epidermis?
A
Protects mitotically active cells from DNA damage by producing melanin
10
Q
What is the thickest layer of skin? Which cell type is found here?
A
Stratum spinosum; keratinocytes.
11
Q
Name 5 functions of the skin
A
- Protection (against pathogens and UV light)
- Thermoregulation (adipose, sweat glands, hair)
- Metabolism (vitamin D production)
- Cutaneous sensation
- Physiological
12
Q
Name 5 factors which make burn sites an ideal environment for infection
A
- Loss of intact skin barrier
- Necrotic skin provides great culture medium
- Oedema reduces blood supply to the area
- Reduced immunoglobulin levels right after the burn
- Hypovolemia –> hypotension –> hypoxia (natural response)
13
Q
What is the most effective method of preventing infection in burns? Why?
A
Debridement/escharotomy - gets rid of dead tissue/culture medium
(following patient stabilisation and burns demarcation)
14
Q
Describe what is involved in the infection control procedures for burns patients
A
- Single-patient rooms (for >20% open wounds)
- Hand hygiene
- PPE
15
Q
Describe what is involved in the surveillance policies for burns patients
A
- Routine wound, sputum, and urine cultures
- Identifying episodes of cross contamination
This helps guide empiric antibiotic treatment, e.g. if the patient does develop an infection days-weeks later, we know what organisms were present
16
Q
What is the gold-standard investigation in un-excised burns?
A
Histology
Tissue biopsy is graded from 0-IV
17
Q
What are the most common causative organism in burns infections for:
- Early infections
- Mid-term infections
- Late infections
A
EARLY: gram-positive organisms such as Staph aureus, streptococcus pyogenes
MIDDLE: gram-negative Ps. Aeruginosa
LATE: multi-resistant organisms & fungal infections (e.g. candida, aspergillus)
https://www-uptodate-com.proxy.library.adelaide.edu.au/contents/burn-wound-infection-and-sepsis?search=burns%20infection&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H372573676
18
Q
Name 4 other non-local infection complications
A
- Bloodstream infections
- Pneumonia (e.g. inhalation injury)
- Endocarditis
- UTI
19
Q
Name the 2 factors that affect burn severity
A
- Depth of burn
2. Surface area
20
Q
Give an example of thermal and non-thermal burns
A
THERMAL: contact with fire
NON-THERMAL: electrical burn, radiation burn, chemical burn
21
Q
How can burns cause compartment syndrome?
A
Circumferential burns or eschars cause loss of skin elasticity, impairing blood flow
This can then cause compartment syndrome due to fluid accumulation
22
Q
How can the surface area of burns (TBSA) be calculated?
A
- Lund-Browder chart (for adults and children) - note that superficial/first-degree burns are not included in percentage TBSA assessment
- Wallace’s rule of 9s (for adults)
- Palm method (least accurate)
23
Q
Time frame when cool running water is still effective?
A
<1 hour
but evidence is not conclusive
24
Q
What are the major threats to life in a severely-burned patient? (name 5)
A
- Shock/Hypovolemia
- Infection
- Hypothermia
- Pneumonia (from inhalation injury)
- Systemic inflammatory response –> compromises organ perfusion
25
How is the depth of burns assessed?
1st, 2nd, 3rd, 4th degree classification was replaced by a system reflecting the need for surgical intervention:
```
Superficial/epidermal
Superficial partial-thickness
Deep partial-thickness
Full-thickness
Deeper injury
```
(figure 1: https://www-uptodate-com.proxy.library.adelaide.edu.
au/contents/assessment-and-classification-of-burn-injury?search=burns&source=search_
result&selectedTitle=2~150&usage_
type=default&display_rank=2#H10)
26
When is surgical intervention required? (according to depth of burn)
Deep partial-thickness and beyond
27
Describe the appearance of a superficial/epidermal burn
| 1st-degree
Dry, red
Blanches when touched
Painful
https://www.nature.com/articles/s41572-020-0145-5
28
Describe the appearance of a superficial partial-thickness burn
(2nd-degree)
Moist, red, weeping
Blisters
Blanches with pressure
Painful to temperature, air, and touch
Only affects the dermal papillary layer
29
Describe the appearance of a DEEP partial-thickness burn
| 2nd-degree
```
Blisters (easily unroofed)
Waxy/wet
Variable in colour from red to white
Blanching with pressure may be sluggish
Painful to pressure ONLY
```
Affects the dermal papillary AND reticular layer
30
Describe the appearance of a FULL-thickness burn
| 3rd-degree
Waxy white to leathery gray to charred and black
Dry and inelastic
No blanching with pressure
Painful to DEEP pressure ONLY (no pinprick or light touch sensation)
Epidermis AND dermis affected
31
Describe the appearance of a deeper injury burn
| 4th-degree
Extends into fascia and/or muscle and bone (hypodermic layer)
Sensation: deep pressure only
32
What is a pressure garment used for?
Maintaining alignment of collagen fibres whilst the burn is healing.
Helps reduce scarring.
33
When is airway management/intubation indicated?
- If an inhalation injury is suspected
| - If burns involve >30-40% of the body surface
34
Prolonged cooling of a larger TBSA (>9%) can cause...?
Hypothermia
35
What are the 3 components of inhalation injury?
1. Upper airway swelling (occurs 12-24 hours after initial burn injury)
2. Acute respiratory failure
3. CO intoxication (due to smoke inhalation)
36
List 4 signs of inhalation/upper airway injury that would prompt intubation.
- Voice changes!
- Cough
- Stridor
- Inspiratory grunting
- Tachypnoea
- Wheezing
- Burn distribution: i.e. above the clavicles, involving the face, burns to the nose, nasal hairs, mouth, pharynx
37
Why is intubation recommended as opposed to observation for upper airway injury?
Natural Hx of upper airway injury: it causes oedema and narrowing of the airway within 12-24 hours
38
There are many systemic effects of large (>30% TBSA) burns injuries. List 5 of these.
1. Systemic inflammatory response
2. Evaporative fluid loss leading to hypovolemia and hypothermia
3. Haemolysis & muscle damage
4. Immunosuppression
5. Hypermetabolic state
39
Outline the pathophysiology and consequences of systemic inflammatory response syndrome
1. Release of cytokines & inflammatory mediators
2. Increased vascular permeability
3. Extravasation of intravascular proteins and fluid into interstitial tissue
RESULTS: tissue oedema, hypovolemic shock, acute respiratory distress syndrome, paralytic ileus, disseminated intravascular coagulation (DIC)
40
Describe 3 clinical features that may be present in a severely-burned person
1. Clinical features of SHOCK: hypotension, tachycardia, poor urine output, prolonged cap refill
2. Clinical features of ARDS: dyspnoea
3. Clinical features of inhalation injury / upper airway injury: tachypnoea, wheeze, stridor
4. Compartment syndrome / acute limb ischaemia: 5 P's (pallor, pulselessness, parasthesia, paralysis, pain)
41
Outline the acute/immediate management of severe burns
1. AIRWAY: intubation and high-flow oxygen (if indicated)
2. Fluid resuscitation
3. Management of burn area (e.g. removing burnt clothing, cooling and covering the burn area)
4. Analgesia
5. Tetanus prophylaxis
42
Fluid resuscitation is adjusted to maintain urine output at...?
1. 0 mL/kg/hour for children
| 0. 5 - 1 mL/kg/hour for adults
43
What is an escharotomy?
A surgical procedure used to treat full-thickness (third-degree) circumferential burns
Incision down to the subcutaneous fat in order to allow underlying structures to expand - prevents further tissue injury
44
Why is a burn a 'dynamic' injury?
It can change in size and depth over time (explained by the theory of Jackson's burn wound model)
45
Describe Jackson's burn would model
https://www.racgp.org.au/afp/2017/march/burns-dressings/
3 zones:
1. Zone of coagulation (dead: irreversible coagulative necrosis)
2. Zone of stasis (damaged but viable tissue with decreased perfusion. The target area for burns treatment; prevent progression to coagulation)
3. Zone of hyperaemia (inflammation and increased blood flow)
46
How can burns cause asphyxiation?
Compressive eschar around the neck or chest --> restricts chest excursion --> asphyxia
47
What is Postburn hypermetabolism and when does it occur?
Initial hypometabolism (ebb state) followed by hypermetabolic state (flow state): occurs in patients with moderate-severe injuries
Hypermetabolic state onset ~5-7 days post-injury and can last for up to three years
48
What is the hypermetabolic flow phase characterised by?
- Hyperdynamic circulation
- Insulin resistance
- Protein & lipid catabolism
- Increased resting energy expenditure
- Increased body temp
- Muscle wasting
- Simulated synthesis of acute-phase reactants
BASICALLY JUST A CATABOLIC STATE
49
In the first 48 hours following a burn injury, pathogens from which areas colonise and cause infection?
Staphylococci from the sweat glands and hair follicles
50
In the 5-7 days following a burn injury, pathogens from which areas colonise and cause infection?
GIT
Upper respiratory tract
Hospital environment
51
What are the 2 methods of wound healing? Describe what is involved in each.
1. Regenerative (primary intension): tissue replaced with parenchymal tissue (e.g. fracture)
2. Non-regenerative (secondary intension): healing occurs by replacement with connective tissue scar (e.g. MI). Tissue is NOT replaced with functional parenchymal cells.
52
Using the ABCDE primary survey, outline the concerns and treatments that can be implemented in someone with significant burns.
ATTS = analgesia, tests, tubes (e.g. NG, indwelling catheter), secondary survey
https://trauma.reach.vic.gov.au/guidelines/burns/primary-survey
53
When can you use glad wrap?
Within the first 12-24 hours as a transfer dressing
| DON'T USE IT ON THE FACE YOU'LL SUFFOCATE THEM LOL
54
Difference between an escharotomy vs. a escherectomy?
Escharotomy: cutting into the skin for decompression
Escharectomy: removing the entire thing
55
What is the Parkland formula? How is it used?
Parkland formula: 3-4mL/kg/% of burn/24 hours
1/2 in the first 8 hours from the time of injury
1/2 in the next 16 hours
E.g. in an 80kg person with 25% TBSA burns: 4mL x 80 x 25 = 8000mL (8L): 4L in first 8 hours, 4L in next 16 hours.
However it is important to note that there may be an increased risk/exacerbation of laryngeal oedema or compartment syndrome if present. In this case the modified Parkland formula may be used where instead of 4mL, the volume is calculated using 2 or 3 mL.
56
Oedema occurs in all burned areas. When does oedema occur in NON-BURNED areas?
When TBSA of burns exceeds 25%
57
Explain the changes that occur at a capillary level when someone suffers a burn. How does this cause oedema?
INFLAMMATORY METABOLITES and DAMAGE FROM THE BURN = leaky capillaries
Na+, proteins, and fluid shift from the intravascular into the interstitial space.
58
TISSUE COMPLIANCE:
Proteins become denatured. When the proteins are damaged in the ICM, there is a vacuum that draws fluid OUT and you leak fluid.
Burned tissue will swell dramatically but whole body will swell more because the capillary is leaking ADDITIONAL fluid. It SUCKS fluid out of the adjacent capillary bed.
TISSUE COMPLIANCE:
Proteins become denatured. When the proteins are damaged in the ICM, there is a vacuum that draws fluid OUT and you leak fluid.
Burned tissue will swell dramatically but whole body will swell more because the capillary is leaking ADDITIONAL fluid. It SUCKS fluid out of the adjacent capillary bed.
59
How can circumferential burns be treated (initially and later in management)?
Start with ELEVATION to reduce oedema
THEN an escharotomy (especially if you are a few hours away from more advance help)
60
Factors that increase the time of exposure to a burn and increase the depth of burn
- Intoxication
- Clothing
- Viscosity (e.g. hot oil vs. flame)
61
What percentages make up wallace's rule of 9s
```
Head & neck = 9%
Arms (2 x 9) = 18%
Trunk = 18%
Trunk (Back) = 18%
Legs (18 x 2) = 36%
Perineum = 1%
```
62
What is Hartmann's solution and how does it differ from saline?
Hartmann's solution is a crystalloid solution that is closely isotonic with plasma.
It contains electrolytes and lactate (which helps generate alkalising bicarbonate). It is more 'physiological' than saline.
63
What issues are caused by an eschar?
Leaving dead tissue in a deep burn facilitates bacterial colonisation and drives deterioration/deepening of the burn.
Removal helps address the negative hydrostatic pressure across into the interstitial space --> less oedema
64
How is burn depth assessed?
insert some flow chart
Epidermal integrity --> slippery --> colour or blister thickness, etc.
It's in ur screenshots
65
What is Nikolsky's sign?
Dislodgement of intact superficial epidermis by a shearing force.
If the sign is positive, the first layer of skin will shear off.
66
When is Hartmann's Solution preferred over normal saline in IV resuscitation for burns?
When TBSA > 20%
67
```
Name one (1) Gram positive and one (1) Gram negative microorganism that cause multi-drug resistant
infections of burns.
```
Gram-positive: staphylococcus aureus
Gram-negative: pseudomonas aeruginosa
68
Outline the primary survey to be undertaken for a burns patient.
AIRWAY: inhalation injury (soot, facial burns, hoarse voice, singed nasal hairs, etc.), contaminants in the mouth, airway patency
BREATHING: work of breathing, effectiveness of breathing, stridor, wheeze, circumferential burns that may be inhibiting chest wall movement, ARDS
CIRCULATION: signs of shock/hypovolemia (HR, BP, temperature, cap refill), carbon monoxide poisoning
DISABILITY: AVPU, altered mental status (e.g. due to CO inhalation), head injury
ENVIRONMENT/EXPOSURE: check how much of the body is burned (calculate %TBSA)
69
Why is IV fentanyl the preferred analgesia for severe burns?
Fast-acting pain relief (1-2 minutes)
Also less likely to induce NV
Morphine is renally-cleared and may not be suitable if a burns patient is suffering AKI from hypoperfusion
70
What should be carefully monitored in patients receiving opioids?
Respiratory depression
CNS depression
Dependence
71
Outline the investigations that would be required for a burn injury
PULSE OXIMETRY - monitor for hypoxemia (CO inhalation will not affect pulse oximetry)
BLOOD GASES - monitor for hypoxemia and respiratory or metabolic acidosis
SERUM ELECTROLYTES - hyperkalemia and hyponatremia in the acute phase
CXR: rule out ARDS
CARBOXYHAEMOGLOBIN LEVELS: check for CO poisoning
SERUM PROTEIN AND ALBUMIN: hypoalbuminaemia in the acute phase after a burn
72
Why are pulse oximetry values unaffected (or falsely high) in carbon monoxide poisoning?
Complexes of Hb and oxygen and complex of Hb and carbon monoxide are indistinguishable.
73
What is ARDS?
A severe inflammatory response of the lungs to pulmonary damage
74
Name a defining laboratory feature of ARDS and explain what it represents
PaO2/FiO2 ratio <300mmHg
This is the ratio of arterial oxygen partial pressure (measured by ABG) to fractional inspired oxygen (FiO2).
75
What is a normal PaO2/FiO2 ratio?
PaO2/FiO2 ratio >500mmHg
76
What is the pathophysiology behind ARDS?
1. Pulmonary damage
2. Inflammatory response
3. Neutrophils move into alveoli
4. Excessive release of neutrophilic mediators
5. Diffuse alveolar damage
Clinical manifestations: decreased pulmonary compliance, hypoxemia, respiratory distress, hyperventilation
77
What are the clinical features of ARDS?
Acute dyspnoea, tachycardia, tachypnoea
Cyanosis
Diffuse crackles
Possible: fever, cough, chest pain
78
What acute findings may be present on the CXR of someone with ARDS?
Diffuse bilateral symmetrical infiltrates
| note that CXR may be normal in the first 24 hours
79
How can a CXR resembling ARDS be distinguished from CHF?
- History
| - Other investigations: ABG, echocardiography, CT chest, etc.)
80
Why are serum protein levels low after a significant burn injury?
Higher vascular permeability (at the site of the wound and possibly also due to SIRS) produces exudation
81
What measures can be taken to prevent the patient from losing heat during surgery?
Warm IV fluid
Heated operating theatre
82
Why does gentamicin require such careful monitoring of renal function and gentamicin concentrations?
Ear toxicity - can get hearing loss
Reversible kidney damage (100% really cleared) but irreversible ototoxicity
83
What is biobrane?
A biosynthetic skin dressing that mimics the properties of skin and doesn't tear.
Stretchable, provides temporary cover for clean partial thickness burns or over split skin grafts.
84
What is a split skin graft?
A split skin graft (SSG) is where a very thin shaving of normal, healthy skin is used to cover an area of skin that has been damaged or cannot heal because of an injury (e.g. a severe burn).
85
What does meshing of a split skin graft involve?
Poking holes in the skin graft so that it can be stretched over a larger surface area (for larger injuries)
86
Which factors contribute to hypovolemic shock and potentially end-organ damage in a burns patient? (3 things)
1. Loss of fluid through evaporation (no skin barrier)
2. SIRS or inflammatory factors --> increased capillary permeability --> fluid leakage into interstitial and third space
3. Potential infection --> sepsis --> increased capillary permeability
87
Why do burns patients develop hyperkalemia?
Ischaemia and necrosis of muscle cells --> release of intracellular contents (potassium)
88
Why is intubation performed before commencing fluid resuscitation?
Because fluid resuscitation can worsen laryngeal edema, intubation should be performed before fluid resuscitation!
89
Initial management and management of complications
```
INITIAL MANAGEMENT:
Pain control
Debridement/Escharectomy
Intubation
Fluid management
```
MANAGING COMPLICATIONS:
Hypovolaemia and Shock [Potential end organ failure]
Lungs – respiratory failure
Local oedema and protein loss
Fluid and electrolyte changes and requirements in treatment
Renal adjustments and consequences in burns patients
Infection and infection control
Nutritional requirements
Trace element needs
90
Why do burns patients develop raised creatinine levels?
Acute kidney injury
91
A slippery burn indicates which burn thickness?
Superfichttps://www.brainscape.com/l/dashboardial dermal
Mid-dermal
(will have blisters)
92
A non-slippery burn indicates which burn thickness?
Deep dermal
Full thickness
93
Name the predominant Gram-positive and Gram-negative organisms cultured from burn sites.
Gram-positive: staphylococcus aureus
Gram-negative: pseudomonas aeruginosa
94
Where do infective organisms arise from? (group according to timeline of burn)
EARLY: commensal skin organisms (e.g. staphylococcus aureus, strep progenies), respiratory tract, environment
2-4 DAYS POST-BURN: Gram-negative organisms (e.g. p. aeruginosa, E. Coli). Skin, upper respiratory tract, GIT, hospital.
Gram-negatives dominate after day 5.
95
The development of which type of vitamin deficiency can occur in full-thickness burn injury?
Vitamin D deficiency
