Burns (1)

Question 1

What is the most common type of burn?
→ What does the extent of it depend on?
→ What can cause it?

What is another type of burn?
→ What are the 2 types of it? How do they differ?
→ How is it managed?

What is another type of burn?
→ What are the 2 types of it?
→ Which type is more severe and why? What are its complications?
→ How is it managed?

Answer 1

➊ Thermal (90%)
→ Temp and duration of the application
→ • Scalds (wet heat) tend to be partial thickness
• Dry heat caused by direct contact, flame, or radiant heat tend to be deep

➋ Chemical
→ • Acid burns cause damage by coagulative necrosis – Local and short-lived
• Alkali burns cause progressive liquefactive necrosis – Deep and prolonged e.g. cement burns
→ Remove clothing and dilute the chemical

➌ Electrical
→ • Low voltage burns (caused by domestic electricity)
• High voltage
→ High voltage as there is an entry and exit point of the burn, therefore anything in between can get damaged:
• Extensive tissue damage
• Asystole and arrhythmias
• Rhabdomyolysis
• Compartment syndrome
• Renal failure
→ ECG monitoring and Serum cardiac enzymes

Question 2

What is the most serious worry with those in a fire?

How does CO affect Hb-O2?

How are those with this injury managed?
→ Why is this effective?

Answer 2

➊ Inhalation Injury (smoke contains noxious products of combustion e.g. soot, CO)

➋ CO has a much higher affinity with Hb than O2, therefore will be preferred over O2 when present

➌ HF O2
→ COHb has a ½ life of 4 hrs in air, but 30 mins in O2, so HF O2 gets rid of the CO much faster

Question 3

What is the local response to a Burn?

Answer 3

• Zone of coagulation – tissue necrosis centrally due to tissue destruction by injury
• Zone of stasis/ischaemia – can progress therefore increasing area of necrosis or depth of injury
• Zone of hyperaemia/inflammation – due to increased vascular permeability, and the inflammatory mediators also cause oedema and thrombosis

Question 4

Systemic Response to a Burn:
What occurs in those larger burns?
→ What affects does this have?

Answer 4

(>25-30% TBSA) Mediators are released into the circulation
→ • Burn Oedema = Oedema of burned tissue and non-burned tissue
o Protein loss peaks at 8-12 hrs
• Impaired microvascular integrity
o Physical gaps between endothelial cells
o Vasoactive substances released i.e. PG, LT, Histamine, F. rads.
o Hypovolaemia
o Myocardial depression
o Red cell destruction – up to 40% of circulating volume
o Glucose intolerance

Question 5

Depths of Burn:
What occurs in Erythema?

What occurs in Superficial partial thickness?

What occurs in Deep partial thickness?

What occurs in Full thickness?

Answer 5

➊ Epidermal damage, no skin loss, heals within days w/o scarring

➋ • Mainly epidermal loss
• Moist, blistered, blanching, very painful
• Heals within 3 wks w/minimal scarring

➌ • Germinal layer epidermis lost
• White/red, no blanching
• Prolonged healing by migration of epidermal cells from burn area
• Scarring, and sometimes/often needs skin grafting

➍ • Loss of entire dermis
• Leathery, no sensation
• Won’t heal unless very small, will have scarring and contractures and needs skin grafting

Question 6

What are the early complications?

Answer 6

• Impaired renal function
• Haemoglobinuria
• Infection and impaired immune function
• Pulmonary damage
• Burn encephalopathy
• Toxic Shock Syndrome
• Malnutrition