CSI 19- Acutely unwell Adult Flashcards

1
Q

what is characterised as a major burn? and what percentage is more likely to affect wider systemic part of the body?

A

major = 15%

systemic = 25%

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2
Q

Epidemiololgy

How do most burns occur?

A

Most common admission cause is a scald

Major burns = flame

Mostly accidental

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3
Q

What risk factors would increase your chance of having a major burn?

A

Low economic status

grils having domestic roles

old age ; frail

overcrowding

psychiatric illness

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4
Q

what is used as a risk prediction to check mortality of burn?

give name and details esp point of futility

A

Revised Baux score

takes into account age, TBSA and presence of inhalation injury.

Point of futility: where mortality approaches 100%, it was 100 before but now 160.

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5
Q

what other risk prediction tools are used in burns

A
  1. Belgian Outcome in Burn Injury
  2. abbreviated Burn Severity Index
  3. Clinical frailty scores
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6
Q

Outline the layers of the skina nd it’s function

A

Epidermis needs dermis to regenerate every 2-3 wks

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7
Q

outline the different classification of burns in terms of severity

A

Epidermal (1st degree)

Superficial partial-thickness

Deep partial-thickness

3rd degree (full thickness)]

fourth degree ( to bone)

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8
Q

what factors affect severity of burns?

A
  • wet scalds (more heat than dry scald )
  • age
  • if first aid was given early
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9
Q

outline the pertinent differences between the classification of burns.

A

superficial: can heal without scarring in 1-2 weeks.

deep: lost dermal vascular plexus and hence managed by excision and grafting.

can also lead to compartment syndrome and rhabdomyolsysis

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10
Q

Outline the local effects of major burns

A

Local events are divided into 3 zones.

Zone of coagulation: dead tissue

Next zone of stasis: hypoperfusion secondary to vasoconstriction and hence vulnerable to ischaemia and necrosis.

Zone of hyperaemia and vasodialtion

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11
Q

outline the systemic effects of a burn

A

Acute phase up to 48hr after injury due to:

  • peripheral vasodilation
  • hypovolemia
  • myocardial depression

leads to shock and hypermetabolic phase that last til 1 year.

Hence early wound excision is better to decrease necrotic load

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12
Q

Initial management of burns

Describe how you will perform first aid

A

Cooled immediately under running cool water for atleast 20 min.

Use SAFE approach (shout, assess, flee danger and evaluate)

Although burn area should be cooled, the rest of the pt should be warmed

Acid burns irrigated for 45 min and alkali fro 1 hr

Use ABCD approach (ATLS)

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13
Q

How can the airway and breathing be compromised in burns

A

inhalation injury

Ventilation

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14
Q

what are the indications for intubation in burns pt

A

Reduced GCS due to:

  1. systemic toxicity from inhalation injury
  2. head trauma from escape

Actual or impending airway obstruction due to deep neck or intraoral burns and oedema

Resp distress

Safe Transfer to burns center

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15
Q

How can ventilation be impaired in burns and give treatment

A

dead tissue non-complaint and cant ventilate and reduce pre-load

  • need escharotomies before transfer

Hypoxameia can occur due to CO poisoning

  • need 100% O2 until carboxyhaem is less than 3%

Hydrogen cyanide poisoning should be considered esp with inhalation injury

  • treat with hydroxycobalamin
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16
Q

Explain how inhalation injury can occur and symptoms

A

Hot gas particles burn the upper airway directly

particulate matter enter lower airway

CO and HCN can cause systemic toxicity

symptoms:

  • facial burns
  • horasness of voice and stridor
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17
Q

how do you manage inhalation injury?

A

Intubate but prepare for difficult airway due to ulceration and oedema

Mitigate by:

  • Giving Suxamethonium up to 48h post-burn
  • Video laryngoscope be used
  • uncut tracheal tube to allow for further soft tissue swelling
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18
Q

Explain how you would manage the circulatory problem associated with burns

A

Assess for hemodynamic instability.

use 2 large bore (14G) cannula.

Use parkland formula (3mls) for resus

  • ½ in first 8 hr and 1/1 in remaining 16
  • subtract any fluid given already
  • use warm isotonic crystalloid

for maintenance : use parkland formula

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19
Q

what causes low GCS in burns? esp at presentation

A

CO and HCN

trauma

medical comorbidities

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20
Q

Outline the principles in estimating exposure in burns

A

All clothes be removed,

reduce exposure due to hypothermia

erythema alone is not sufficient

Do not overestimate as it can affect parkland

Use rule of nines or even better the Mersey burns app

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21
Q

what is involved in the secondary survey in burns

A

Corneal damage: assess using flouresciene

CK needed for rhabdo esp in electrical burns

Tetanus toxoid treatment

Pain relief using IV opioids

NG tube for gastric decompression

22
Q

Outline the procedure for escharotomies?

A

escharotomies: surgical excion through on compliant full thickness BURN

Should be performed as soon as they require ventilation

Incisional incision from unburned skin to unburned skin

Anaesthesia and diathermy used.

Add Abx

23
Q

how are echarotomies different from fasciotomies

A

fasciotomies are deeper as it passes through the muscle fascial layer

Indicated in compartment syndromes commonly caused by high V electrical burns

24
Q

Algorithm for fluid therapy:

Outline it if there’s no hypovolemia and no need for fluid resus

A
25
Q

what are the indications that a pt may need fluid resus

A

Assess volume status taking into account clinical examination, trends and context.

Indicators that a patient may need fluid resuscitation include:

  • systolic BP <100mmHg;
  • heart rate >90bpm;
  • capillary refill >2s or peripheries cold to touch;
  • respiratory rate >20 breaths per min;
  • NEWS ≥5;
  • 45o passive leg raising suggests fluid responsiveness
26
Q

outline algorithm if they DO need fluid resus

A
27
Q

if pt doesn’t have complex fluid or electrolyte replacement of distribution losses, outline the algorithm for routine maintenance

A

Give maintenance IV fluids Normal daily fluid and electrolyte requirements:

  •  25–30 ml/kg/d water
  •  1 mmol/kg/day sodium, potassium*, chloride
  •  50–100 g/day glucose (e.g. glucose 5% contains 5 g/100ml).

Reassess and NGT is preferable when maintenance needs are more than 3 days

28
Q

Outline algorithm 4 when there’s abnormal losses and distribution

A
29
Q

Algorithm 4

How do you check for existing fluid or electrolyte deficits or excess

A
30
Q

Algorithm 4

How do you check if there’s ongoing losses and hence estimate the amount?

A

Check for:

  • vomiting and NG tube loss
  • biliary drainage loss
  • high/low volume ileal stoma loss
  • diarrhoea/excess colostomy loss
  • ongoing blood loss, e.g. melaena
  • sweating/fever/dehydration
  • pancreatic/jejunal fistula/stoma loss  urinary loss, e.g. post AKI polyuria.
31
Q

Algorithm 4

How do you check if there’s Redistribution losses and complex issues

A

Check for:

  • gross oedema
  • severe sepsis
  • hypernatraemia/ hyponatraemia
  • renal, liver and/or cardiac impairment.
  • post-operative fluid retention and redistribution
  • malnourished and refeeding issues

Seek expert help if necessary and estimate requirements.

32
Q

how much fluid is reabsorbed by the blind-ended lymphatic system per day

A

3L

33
Q

outline how burns can lead to distributive shock, cardiogenic and hypovolameic shock

A

Distributive: most common type

Hypovolaemic: evaporation

Cardiogenic: cardiac stress due to less venous return esp in full-thickness burn. and TNF-a reduces cardiac contractility.

34
Q

what is the difference between hypovolaemic and distributive shock?

A

Hypovoalemic: fluid/plasma is ACTUALLY LOST FROM body

Distributive: fluid is redistributed elsewhere in the body and leads to intravascular depletion.

35
Q

explain how obstructive shock can occur and five examples of causes

A

something within the circulation is blocking flow to tissues and lead to flow.

e.g:

  • acute pericardial tamponade,
  • tension pneumothorax,
  • pulmonary or systemic outflow obstruction
36
Q

Breakdown the different types of causes: circle picture

A
37
Q

after inital resus of burns (incl ABCDE), what must you consider?

A
  • Admission to specialist : depends on TBSA (10-20%) and depth of burn (full thickness), face burns or circumferential burns
  • Ongoing fluid resus
  • Supportive care in ICU esp with nutritional support or inhalation injury
  • Tetanus
  • Surgery (full partial thickness) or compartment syndrome which will require fasciotomy or escarotomies
  • VTE prophylaxis
  • Pain and anxiety
38
Q

outline the rule of nines

A
39
Q

what are the similarities and differences beteen partial thickness and intermediate thickness burns

A

Intermediate need surgery and will scar, partial will not

Both blister and weep

Increased risk of infection the deeper it is

40
Q

outline the features of 3rd and 4th degree burns

A

Dry and insensate

High risk of infection and will need grafting

Lead to contracture

4th: to bone and complete loss of burnt part

41
Q

Outline how these fluid types will redistribute in the body fluid compartments in a normal healthy adult and explain why:

  • 1L saline
  • 1L dextrose
  • 1l Hartmann’s / Ringer’s Lactae
A

1L 5% dextrose:

  • Need fluid in intravascular space
  • Assumption is that glucose transporters are passive
  • It will split 2/3 intracellular and 1/3 extracellular
  • Not good for burns as it does not bulk up the extravascular space

1L saline 0.9%

  • Cells cannot take up Na as the Na+/K pump expels ALL Na back out
  • Fluid builds up in interstitial space and hence in blood
  • Good for burns and preserves volume as it is split 75-25
  • Problem is the more you administer, the more you dilute bicarb in the blood (lose buffering capacity) and hence can lead to hypercholreamic acidosis
  • Much cheaper to use and more widespread is used.

Ringer’s lactate/Hartmann’s

  • It generates bicarb an prevents hyperchloreamic acidosis
  • Concentration of Hartmann’s is lower than saline and hence will enter cells
42
Q

Why is colloid not used widespread and explain it’s distribution

A

100% should enters plasma but not seen in practice.

Problems:

  • could cause problems in widespread inflammation.
  • It can cause allergy and anaphylaxis hence it is phased out.
43
Q

outline the psych effects of burns

A

Facial burns cosmetics

Hand burns esp dominant- not good if you play music

PTSD symptoms:

  • Hyperarousal
  • Dissociation
  • Avoidance
  • Insomnia
  • Hypoarousal
  • Flashbacks
44
Q

what are the features of the hypermetabolic state?

A

by a hyperdynamic circulatory response with esp with those with 40% TBSA:

  • massive protein and lipid catabolism, total body protein loss
  • muscle wasting,
  • peripheral insulin resistance,
  • increased energy expenditure,
  • increased body temperature,
  • increased infection risks, and
  • stimulated synthesis of acute phase proteins located in the liver and intestinal mucosa.

it starts within 5 days and persist up to a year

45
Q

describe and explain the 2 distinct patterns of metabolic regulation post injur

A

ebb phase:

  • occur within 48 hr
  • decreased CO, O2 consumption and met rate
  • impaired Glucose tolerance and hyperG

Flow phase:

  • gradual increase in metabolism within first 5 days
  • insulin release is twice normal but glucose stays high due to resistance.
  • hyperdynamic circulation and hypermet state.
46
Q

Explain glucose metabolism in hypermetabolic state

A

Stress response: cortisol and catecholamines do their job

However hyperglycaemia FAILs to suppress hepatic glucose output and insulin effect is attenuated a lot

catecholamines affect GLUT-4 therefore affecting peripheral insulin resistance

47
Q

Explain protein and lipid metabolism in a hypermetabolic state

A

iN BURNS , pts cannot metabolise fats and ketones

Hence loss of lean muscle is needed to provide energy due to inflammation (mediated by TNF-a)

may even contribute to insulin resistance

this can affect development in children

48
Q

Outline the pharmacological interventions to slow the hypermetabolic state (even in kids) in acute and chronic

A

Analgesia: IV opioids and psychotherapy for anxiety

Oxandrolone: testosterone analog to reduce loss of lean muscle (even in kids)

Insulin acutely : IN SEVERELY burned pts with diabetes and target should be between 110-150.

GLP-1 agonist: those without diabetes

Metformnin

Growth hormone: kids alone and chronic and do not use infection or sepsis

Propanolol: stop catecholamines which lead to insulin resistance

49
Q

Outline the NON-Pharmacological interventions in hypermetabolic state

A

Early wound closure using autologous grafts

For those with moderate to severe burns - increase ambient temp to 33C to reduce resting energy expenditure

A balanced physical therapy is needed to restore metabolic variables and improve outcomes

High caloric (high carb/lowfat) nutritional support via enteral feeding

  • burn pts cant store fat as VLDL or even metabolsie it
50
Q

what is the formula to calculate energy expenditure

A

Currie formula

51
Q

what are the different types of grafts?

A

Xenograft: another species and only used on a temporary basis

Autografts: pts own uninjured skin and the mainstay.

Isograft: from identical twin

Allograft: used with TBSA over 40%. derived from cadavers. Can lead to rejection