Red Book - Burns Flashcards
Pathophysiogy of major burns
Classify
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 area
Rule of nines
Using 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
Features of airway
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
Intubagtion features
Use at least a size 8 tube
Uncut tube - oedema!
Lung protective vent
ABG, CO and cyanide levels
What determines fluids
Parkland formula
Volume = 4ml x weight x TBSA
Half in first 8 hours, half over 16 hours
(Minus anything already given)
Management priorities
Airway
C-spine (depending on mechanism)
Breathing and ventilation
C - fluids and iv access, catheter and CVP
D - 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 o9f inahlation injury
Early bronch - confirms
BAL and pulmonary toilers
Neb therapy (poor evidence) —> Bronchodilators, Heparin (reduce fibrin), NAC (mucolysis)
Lung protective Vent
ECCO2R, ECMO
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 < 5
Age > 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 syndrome
Infections - 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% O2
Half 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/delated manifestations of neuro
Parkinson type symptoms
