Derm - Burns Flashcards
What are the main pathophysiological processes in burns
1) systemic inflammatory repsonse
2) inhalational lung injury
3) Hypermetabolic state
Describe the inflammatory response
Activbation of inflammatory cascade
Increased vascular permeabilityy
Generalised oedema
WOUND HEALING AFFECTED
IMMUNOSUPPRESSION
INCREASED INFECTION
Patholgical features of inhalation injury
Air obstruction
Oedema
Poor gas exhange
ARDS
Features of hypermetabolic state
Increase protein catabolism
Increased gluconeogenesis
Decreased protein synth
DECRESAED WOUND HEALING
IMMUNOSUPPRESION
INFECTION
Ways of estimating burn area
Lund Browder Chart as % total bodt surface areaRule of ninesUsing palm print and fingers to represent 1%
Assessing burn depth
Superficial, partial and full thickness
Superficial - epidermis Erythema and painful, dry
Partial - (can be superficial or deep dermal) Erythema, pain, oedeam, blisters
Full - All layers and even sub cut structures Painless, white
Concerning features of airway in burns patient
Burns to face
Carbonaceous sputum
Singing of nasal and facial hairs
Oropharyngeal oedeam
Stridor
Voice changes
ALSO Neck burns
Resp failure
Low GCS
To give analgesia or do a procedure
Things to consider for intubation in burns
Use at least a size 8 tube
Uncut tube - oedema!
Lung protective vent
ABG, CO and cyanide levels
What determines fluids in burns?
Parkland formula
Volume = 4ml x weight x TBSA
Half in first 8 hours, half over 16 hours
(Minus anything already given)
Management priorities
AirwayC-spine (depending on mechanism)
Breathing and ventilation
C - fluids and iv access, catheter and CVPD
- temperature - set point reset to 38.5C
- avoid hypothermia
- analgesia - opiates and ketamine
E - Surgical management - debride, escharotomy
Features of the history of concern
When was the fire
Did the patient self extricate (duration of exposure)
Other injuries (blast, jumping from a window)
Nautre of the fire - outdoor/indoor/contained
Chemical/plastics
Patients condition at the scene - GCS, injuries, CPR
What is inhalation injury
Prolonged smoke exposure in a confined space
Composed of UPPER AIRWAY THERMAL INJURY CHEMICAL IRRITATION OF THE RESP TRACT
Upper airway Oedema of the tonuge, lips, pharynx etc Tube early and prophylactically
Chemical Direct injury to epithelium by acidic/alkaline compounds in smoke Causes tracheobronchitis Poor mucociliary clearence Loss of surfactant —> atelectasis
Early inflmaation, and capilary leak - exudate —> ARDS
Management of inahlation injury
Early bronch - confirms
BAL and pulmonary toilers
Neb therapy (poor evidence) —> Bronchodilators, Heparin (reduce fibrin), NAC (mucolysis)
Lung protective Vent
ECCO2R,
ECMO
Burns mortality without and with inhalation injury
13.9 to 27.6%
Define Burn Shock
Combination of: Hypovolaemia Distributive shock Cardiogenci shock In a patient with major burns
Refractory to fluid resus
American Burn Association criterial for sepsis
Documented infection plus:
Temp >39 or < 36.5
RR > 25 (or MV with min vol > 12 l/min)
HR > 110/min
Glucose >12.8 (non DM)
Intolerance of enteral feed in 24 hours
Plts < 100
When to refer to a burns unit
Age < 5Age > 60
Comorbidities that affect healing DM, immunosuppression, Pregnancy, Liver disease/cirrhosis
Site face, hands, feet, perineum flexures - neck/axilla circumferential burns of the torso, limbs, neck
Inhalational injury
Mechanism - Chemical with greater than 5% area Ionising radiation Pressure steam injury Electrical and cold injuries Suspicious/NIA
Dermal/full thickness burns > 5% in under 16 or >10% if >16
Complications of major burns
Over resuscitation Oedema, limb and abdo compartment syndrome Pulmonary oedema, prolonged MV
Resp Obstructions, ARDS
CVS Arrythmias MI, failure, vasoplegia
Neuro PAIN Opioid tolerance (Consider ket, gaba, amitrpyt)
Renal AKI - under resusc ACS/Rhabdo
GI Increased nutrition requirement - hypermetabolism Increased protein catabolism
Haem - VTE
Metabolic - rhabdo, compartment syndromeInfections - burn wound, pneumonia, sepsis (lines and cathter)
MSK - contractures/amputation
Pathophys of Carbon Monoxide
CO is 20x more affinity for Hb than O2
Impaired O2 delivery, reduced carrying capacity
Curve to the LEFT
Additional - impaired cytochrome oxidase, so poor utilisation at mitochondira
Presentation of CO poisoning
N and V, headache
Hypotension
Neuro - mild confusion to seizures
Cherry red skin (rare)
Tests in CO poisoning
Carboxy Hb on a co-oximerter on ABG
(Normal <1%, smokers <5%)
SpO2 goes to 100% (absorption spectra of HbCO similar to HbO2)
Normal PaO2
Management of CO poisoning
100% O2Half life from 4 hours to 1 hour.I &V is HbCO>25%Hyperbaric O2. —> 15-20 minutes half life If: HbO2 >40% Pregnant (HbCO>15%) Coma
Prognosis of CO
Poor relationship betwen HbCO level and the presence/absence of symptoms or outcomes
BUT
HbCO > 60% likely to be fatal
Mechanism of cyanide poisoning
Inhibits cytochrome oxidase at mitochondria
Blocks oxidative phosphoryl.
Leads to anaerobic metabolism
Symptoms of CO poisoning
Breathless
Hypotension
Vomiting
Agitation
LOC
Unexplained metabolic acidoss and high SvCO2
Ix for CO
Lactic acidosis
High ScvO2 —-> low AV gradient
Cyanide level (takes 3 hours)
Tx for cyanide
100% O2
Intubate if needed
ANTIDOTES:
Hydroxycobalamin
Dicobalt edetate
Sodium thiosulphate (converts cyanide to thiocyanide —> renal excretion)
Prognosis of cyanide
Good if rapid therapy and antidotes
Poor if cardiac arrest due to cyanide
Risk of post survival anoxic enceph
Acute/delayed manifestations of neuro
Parkinson type symptoms
What is the difference between a Burn centre, a burn unit and a Burn facility?
Burn Centre: This level of in-patient burn care is for the highest level of injury complexity and offers a separately staffed, discrete ward. The facilities are up to the highest level of critical care and have immediate operating theatre access
Burn Unit: This level of in-patient burn care is for the moderate level of injury complexity and offers a separately staffed, discrete ward
Burn Facility: This level of in-patient burn care equates to a standard plastic surgical ward for the care of non-complex burn injuries
What is a chemical burn?
Chemical burn is a burn to internal or external organs of the body caused by a corrosive or caustic chemical substance that is a strong acid or base
What causes a chemical burn?
The main cause of chemical burn is contact with strong acids or bases.
The strength of acids and bases is defined by the pH scale, which ranges from 1–14.
A very strong acid has a pH of 1 and may cause a severe burn.
A very strong base has a pH of 14 and may also cause a severe burn.
What are some of the common chemical burns?
Sulphuric acid
Nitric acid
Hydrochloric acid
Phosphoric acid
Sodium hydroxide and potassium hydroxide
Ammonia
What are some of the features you would want to illicit from the history?
pH of the agent
Concentration of the agent
Length of contact time
Amount of agent involved
Physical form of the agent (ie: solid, liquid, gas)
Site of contact (e.g. eye, skin, mucous membrane)
Whether swallowed or inhaled
Whether or not skin is intact.
How would you manage a chemical burn?
Basic first aid should be administered as soon as a chemical burn has occurred.
Remove contaminated clothing
Irrigate the affected area with copious amounts of water. Wash for at least 20 minutes, taking care not to allow runoff to contact unaffected areas. It has been shown that irrigation received within 10 minutes of the burn reduces the severity of the wound and time of stay in hospital.
Chemical burns involving elemental metals (lithium, potassium, sodium and magnesium) should not be irrigated with water as this can result in a chemical reaction that causes burns to worsen. These types of chemical burn should be soaked with mineral oil while waiting for medical attention.
