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
