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FFICM > Red Book - Burns > Flashcards

Red Book - Burns Flashcards

1
Q

Pathophysiogy of major burns

Classify

A

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

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2
Q

Describe the inflammatory response

A

Activbation of inflammatory cascade

Increased vascular permeabilityy

Generalised oedema

WOUND HEALING AFFECTED
IMMUNOSUPPRESSION
INCREASED INFECTION

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3
Q

Patholgical features of inhalation injury

A

Air obstruction
Oedema
Poor gas exhange

ARDS

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4
Q

Features of hypermetabolic state

A

Increase protein catabolism

Increased gluconeogenesis

Decreased protein synth

DECRESAED WOUND HEALING
IMMUNOSUPPRESION
INFECTION

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5
Q

Ways of estimating burn area

A

Lund Browder Chart as % total bodt surface area

Rule of nines

Using palm print and fingers to represent 1%

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6
Q

Assessing burn depth

A

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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7
Q

Features of airway

A

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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8
Q

Intubagtion features

A

Use at least a size 8 tube

Uncut tube - oedema!

Lung protective vent

ABG, CO and cyanide levels

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9
Q

What determines fluids

A

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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10
Q

Management priorities

A

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

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11
Q

Features of the history of concern

A

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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12
Q

What is inhalation injury

A

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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13
Q

Management o9f inahlation injury

A

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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14
Q

Mortality without and with inhalation injury

A

13.9 to 27.6%

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15
Q

Define Burn Shock

A

Combination of:

	Hypovolaemia

	Distributive shock

	Cardiogenci shock

In a patient with major burns

Refractory to fluid resus

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16
Q

American Burn Association criterial for sepsis

A

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
17
Q

When to refer to a burns unit

A

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

18
Q

Complications of major burns

A

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

19
Q

Pathophys of Carbon Monoxide

A

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

20
Q

Presentation of CO poisoning

A

N and V, headache

Hypotension

Neuro - mild confusion to seizures

Cherry red skin (rare)

21
Q

Tests in CO poisoning

A

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

22
Q

Management of CO poisoning

A

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
23
Q

Prognosis of CO

A

Poor relationship betwen HbCO level and the presence/absence of symptoms or outcomes

BUT

HbCO > 60% likely to be fatal

24
Q

Mechanism of cyanide poisoning

A

Inhibits cytochrome oxidase at mitochondria

Blocks oxidative phosphoryl.

Leads to anaerobic metabolism

25
Q

Symptoms of CO poisoning

A

Breathless
Hypotension
Vomiting
Agitation

LOC

Unexplained metabolic acidoss and high SvCO2

26
Q

Ix for CO

A

Lactic acidosis

High ScvO2 —-> low AV gradient

Cyanide level (takes 3 hours)

27
Q

Tx for cyanide

A

100% O2

Intubate if needed

ANTIDOTES:
Hydroxycobalamin
Dicobalt edetate
Sodium thiosulphate (converts cyanide to thiocyanide —> renal excretion)

28
Q

Prognosis of cyanide

A

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

FFICM (59 decks)

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