Week 9 Flashcards
How do burns affecr the cardiovascular system?
Results in massive fluid & electrolyte shifts from intravascular spaces to the interstitium
Burns > 40% TBSA cause myocardial dysfunction (more at risk of hypovolaemic shock / burn shock)
↓ cardiac contractility & cardiac output falls within in minutes of injury (prior to decreased plasma volume)
Chemical & vasoactive mediators cause initial arterial constriction followed by vasodilation & ↑ capillary permeability (loss of capillary seal)
What are the key interventions for cardiovascular system after burns
Restoration of intravascular volume is critical – maintains vital organ function (without exacerbating tissue oedema)
Urine output – KEY TO SURVIVAL (So this is the case when an IDC will be inserted to monitor urine output closely i.e. hourly)
Adults – 30-50 ml / hour
Children – 1-2ml / kg / hour (weighing less than 30 kg)
What is the parkland formula for fluid input for the cardiovascular system following burns
4 mls Hartmann’s solution x TBSA% burned x pt. weight (kg)
Alterations in pulmonary function occur due to burns because of:
Systemic response to the burn injury
Inhalation injury
Circumferential full thickness burns
Respiratory insufficiency from burns can occur at two points (leading to respiratory arrest)
- Resuscitation phase – from inhalation injury
2. Acute rehab phase – (10 days – 2 weeks) from infection
Why should Protein intake should increase after burns
to counteract muscle & viscera being used as protein sources while the body is in a hyper-metabolic state
2 types of pain generally experienced after burns
Pain as a result of the injury- chronic from damaged tissue
Acute pain as a result of procedures e.g. wound dressing, occupational therapy, physiotherapy
Pathophysiology of immediate burn pain
Originates from the nociceptors (pain sensing nerves).
Destroyed nerve endings will not transmit pain, but those intact will trigger pain as will those that are regenerating
Pathophysiology of primary hyperalgesia burn pain
The intense inflammatory response also triggers release of chemical mediators that sensitise the active nociceptors
Pathophysiology of secondary hyperalgesia burn pain
Continuous / repeated stimulation of the nociceptive afferent fibres induces a significant increase in dorsal horn excitability leading to increased sensitivity in surrounding unburned skin
Why is Aetiology is a key factor in assessment
Pivotal to burns assessment is determining the causation of the injury: the type of burn
Some chemical burns can be activated by water (which is used in the initial first aid treatment of the wound) & cause further burning & integument damage
Burns are classified according to;
Depth (according to level of dermis & subcutaneous tissue involved)
Extent of body surface
What is the Resuscitative phase of burn injury management
Lasts from burn injury to 72 hours post injury
What is the Rehabilitative phase of burn injury management
Begins 2-3 days after the initial burn injury & lasts until wound closure
What is the Long term rehabilitative phase of burn injury management
Begins after wound closure throughout the patient’s life span
What is the length of the inflammatory phase for burn wounds
Approx 2 weeks
What is the length of the proliferative phase for burn wounds
lasts up to 1 month
Includes collagen synthesis, revascularisation & reepithelialisation (slower rate)
Collagen layers are not organised as they are in other wounds (contributes to excessive scar formation)
What is the length of the maturation phase for burn wounds
lasts 6-18 months (or longer)
New collagen layers are placed & old are broken down
Excessive deposits produce hypertrophic scarring (deep partial & full thickness burns) contract while maturing causing contractures
What is mechanical debridement
(irrigation with specialised pressure, hydrotherapy), wet to dry dressings
Limited in use, painful, good surface cleansing achieved
What is biological debridement
larval therapy
Useful - only dead tissue is removed, dressings need appropriate conditions for larval survival
What is chemical debridement
Useful, can be relatively slow – uses enzymes, fibrinolytic preps
What is surgical debridement under GA
Fast, preferred method
Either tangential excision or fascial excision
What is Topical antimicrobial therapy
Initially, most burn wounds are colonised by gram positive bacteria, after the first week the burnt surface becomes positive with gram negative bacteria
These wounds are colonised as opposed to infected in most cases
Typically burn patients are started on topical antimicrobials to control proliferation of bacteria
What is the Wallace Rules of Nines
part of the assessment tools used when assessing a burns patient
What is the Parkland Formula
Many formulas are utilised but the Parkland Formula is commonly used. 3-4 ml Hartmanns/kg/%burn/24hrs. ½ in the first 8 hours from the time of injury, ½ in the next 16 hours
What is Jackson’s Zones of Burn Injury
Describes the characterstic changes in damaged tissue
What is a Superficial partial-thickness burn
The epidermis is destroyed or injured and a portion of the dermis may be injured.
What is a Deep partial thickness burn?
A deep partial thickness burn involves the destruction of the epidermis and upper layers of the dermis and injury to the deeper portions of the dermis.
What is a Full thickness burn?
A full thickness burn involves total destruction of the epidermis and dermis and, in some cases, the destruction of the underlying tissue, muscle, and bone.
What is Zone of Coagulation
Is the area closest to the site of heat. Blood flow has ceased and the tissue is non-viable
What is Zone of stasis?
Tissue is still seriously damaged but tissue is still viable but there will be signs of vascular occlusion. This
