Derm - Burns Flashcards by Peter latham

What are the main pathophysiological processes in burns

1) systemic inflammatory repsonse
2) inhalational lung injury
3) Hypermetabolic state

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Describe the inflammatory response

Activbation of inflammatory cascade
Increased vascular permeabilityy
Generalised oedema
WOUND HEALING AFFECTED
IMMUNOSUPPRESSION
INCREASED INFECTION

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Patholgical features of inhalation injury

Air obstruction
Oedema
Poor gas exhange
ARDS

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Features of hypermetabolic state

Increase protein catabolism
Increased gluconeogenesis
Decreased protein synth
DECRESAED WOUND HEALING
IMMUNOSUPPRESION
INFECTION

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Ways of estimating burn area

Lund Browder Chart as % total bodt surface areaRule of ninesUsing palm print and fingers to represent 1%

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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

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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

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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

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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)

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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

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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

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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

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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

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Burns mortality without and with inhalation injury

13.9 to 27.6%

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Define Burn Shock

Combination of: Hypovolaemia Distributive shock Cardiogenci shock In a patient with major burns
Refractory to fluid resus

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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.