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Pathophysiology 2 > Burns and Inhalation Injuries > Flashcards

Burns and Inhalation Injuries Flashcards

1
Q

Burns Definition

A

Injury or damage resulting from exposure to fire, heat, caustics, electricity, or certain radiations

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2
Q

Inhalation Injuries

A

Inhalation Injury = Respiratory tract; URT mainly, LRT possible

When smoke inhalation injury is accompanied by a full-thickness or third-degree skin burn, the mortality rate almost doubles.

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3
Q

Smoke

A

Smoke can result from either pyrolysis (smoldering in a low-oxygen environment) or combustion (burning, with visible flame, in an adequate-oxygen environment).

Smoke is composed of a complex mixture of particulates, toxic gases, and vapors.

The composition of smoke varies according to the chemical makeup of the material that is burning and the amount of oxygen being consumed by the fire.

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4
Q

What Kind of Substance does wood, cottom and paper produce when they are burned

A

Aldehydes (acrolein, acetaldehyde, formaldehyde)

Organic Acids (acetic and formic acids)

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5
Q

What kind of substance does polyvinycloride produce when they are burned

A

Carbon Monixide

Hydrogran Chloride

Phosgene

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6
Q

What kind of substance does Polyurethanes produce when they are burned

A

Hydrogen Cyanide

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7
Q

What kind of substance does Flurinated Resins produce when they are burned

A

Hydrogen Fluride

Hydrogen Bromide

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8
Q

What kind of substance does Nitrocellulose Film and Fabrics produce when they are burned

A

Oxides of Nitrogen

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9
Q

What kind of substance does Melamine Resins produce when they are burned

A

Ammonia

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10
Q

What kind of substance does Petroleum Products produce when they are burned

A

Benzene

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11
Q

What kind of substance does Organic Material produce when they are burned

A

Carbon Monoxide

Carbon Dioxide

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12
Q

What kind of substance does Sulfur Continaing Compounds produce when they are burned

A

Sulfur Dioxide

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13
Q

What kind of substance does Fertiizer, Textiles, Rubber produce when they are burned

A

Hydrogen Chloride

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14
Q

What kind of substance does Swimming Pool Water produce when they are burned

A

Chlorine

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15
Q

What kind of substance does Welding Fumes produce when they are burned

A

Ozone

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16
Q

What kind of substance does Metal Works and Chemical Manufactuering produce when they are burned

A

Hydrogen Sulfide

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17
Q

The prognosis of fire victims usually is determined by

A
  1. Extent and duration of smoke exposure
  2. Chemical composition of the smoke
  3. Size and depth of body surface burns
  4. Temperature of gases inhaled
  5. Age (the prognosis worsens in the very young or old)
  6. Pre-existing health status
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18
Q

1st Degree Burns

Clinical Apperance

A

Depth of Burn: First 2-5 layers of epidermis only

Colour/appearance: Red

Skin texture: Normal

Capillary Refill: Yes

Pinprick Sensation: Yes (tenderness & pain)

Healing: In 5 to 10 days with no scarring

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19
Q

1st Degree Burns

A

minimal depth in skin

–Superficial burn; damage limited to the outer layer of epidermis

–Characterized by reddened skin, tenderness, and pain

–Blisters are not present; healing time is about 6 to 10 days

–The result of healing is normal skin

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20
Q

2nd Degree Burns

Clinical Picture

A

Depth of Burn: Involves epidermis and upper third of dermis

Colour/appearance: Red, may be blistered

Skin texture: Edematous

Capillary refill:Yes

Pinprick sensation: Yes (++ pain)

Healing:

In 10 to 20 days with no to minimal scarring

In 25 to 60 days with dense scar formation

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21
Q

2nd Degree Burns

A

Damage extends through the epidermis and into the dermis but is not of sufficient extent to interfere with regeneration of epidermis

If secondary infection results, the damage from a second-degree burn may be equivalent to that of a third-degree burn.

Blisters usually are present. Healing time is between 7 and 21 days

Resultant healing ranges from normal to a hairless and depigmented skin - texture that is normal, pitted, flat, or shiny

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22
Q

Third Degree Burns

A

Will destroy the full thickness of the skin including both dermis and epidermis and can affect the tissue beneath the skin which can become charred and coagulated

Healing can occur after 21 days or may never occur without skin grafting if the burn is large

The resultant damage heals with hypertrophic scars (keloids) and chronic granulation

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23
Q

Third Degree Burns

Clinical Picture

A

Depth of Burn: Entire epidermis,dermisand extends into the subcutaneous fat

Colour/appearance: White / black or brown

Skin texture: Leathery/ charred

Capillary refill: No

Pinprick sensation:No

Healing: No spontaneous healing, will require grafting

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24
Q

Determination of Area - Surface Burns

For Infants

A

Count 18% if the anterior and posterior surfaces of the head and neck are affected

Count 18% for the anterior and posterior surfaces of each upper limb (total is 18% for both upper limbs)

Count 4 times 9 or 36% for the anterior and posterior surfaces of the trunk, including the buttocks (18% per front and back)

Count 6.75% for the anterior and 6.75% for the posterior surfaces of each lower limb as far up as the buttocks (total 36% for both lower limbs)

1 % for groin

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25
Q

Determination of Area - Surface Burns

For Adults

A

The Rule of 9’s applies to Adults

Count 9 % if the anterior and posterior surfaces of the head and neck are affected

Count 9 % for the anterior and posterior surfaces of each upper limb (total is 18% for both upper limbs)

Count 4 times 9 or 36% for the anterior and posterior surfaces of the trunk, including the buttocks

Count 9% for the anterior and 9% for the posterior surfaces of each lower limb as far up as the buttocks (total 36% for both lower limbs)

1 % for groin

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26
Q

Large 3rd Degree Burns Can Lead To

A
  • Large fluid shifts from the vascular compartment due hyperpermeabilityof the microvasculature
    • From cell mediated toxin release
  • Results in
    • Widespread edema (‘burn edema’)
    • Hypovolemic shock (‘burn shock’)
      • Hypovolemia from fluid shifting
  • Coagulopathic changes such as hemolysis and DIC
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27
Q

Burned Skin

A

Will lose it elasticity

Can impair local tissue perfusion

May cause tissue necrosis

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28
Q

If Circumferential Around the Thorax

A

Burns can decrease chest wall compliance“Third spacing”

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29
Q

Tissue Hypoxia

A

–inhalation of toxic gases

–inhalational burns,

–or from inadequate perfusion

30
Q

Surface Burns and Cardiac Instability

A

Early- Decreased CO and Increased SVR

Later- Decreased SVR

31
Q

Surface Burns and Metabolic Changes

A

Initial anaerobic metabolism

Develops a hypermetabolic state

Presents as Catabolic Hypermatabolism

32
Q

Hypermetabolic State

A

Caused by massive catechoalmine release post butn

Can last up to 2 years post burn

33
Q

Hypermetabolic State is Charaterized By

A

–Increased metabolic rates

–Multi-organ dysfunction

–Muscle protein degradation,

–Blunted growth,

–Insulin resistance

–Increased risk for infection

34
Q

Catabolic Hypermetabolism

A

Pt begins to consume blood and muscle proteins

35
Q

Surface Burns and Immune Function

A

Decreased immune function

Possible reduction in WBC formation

36
Q

Surface Burns and CNS

A

Patients tend to reset thermo-homeostatic point (~38 degCelsius or higher) due to the hypermetabolic state

37
Q

Surface Burns and Other Complications

A

–Risk of Pulmonary thromboembolism is high in later stages

–Infection, sepsis, and gangrene can all occur

–Multi-organ system failure & death

–ARDS

38
Q

Anatomic Alterations of the Lungs

Thermal Injury

A

Refers to injury caused by the inhalation of hot gases

Usually confined to upper airway:

Nasal cavity, oral cavity, pharynx (naso/oro/laryngo)

The resultant swelling can cause an emergency airway problem!…

ANTICIPATE!!

39
Q

Anatomic Alteration of the Lungs Thermal Injury

Manifestations

A

Blistering

Mucosal edema

Vascular congestion

Epithelial sloughing

Thick secretions

Acute upper airway obstruction

40
Q

Thermal Injuries and the Distal Airways

A
  • Distal airways are usually spared serious injury because of:
    • Ability of upper airways to cool hot gases
    • Reflex laryngospasm
    • Glotticclosure
  • Direct thermal injuries usually do not occur below the level of the larynx, except in the rare instance of steam inhalation.
  • Damage to the distal airways is mostly caused by a variety of harmful products found in smoke.
41
Q

Anatomic Alterations of the Lungs

Smoe Inhalation Injury

Tracheobronchial Tree and Alveoli

A

–Inflammation of the tracheobronchial tree

–Bronchospasm

–Excessive bronchial secretions and mucous plugging

–Decreased mucociliarytransport

–Atelectasis

42
Q

Smoke Inhalation Injury

Pathological Changes

A

The pathologic changes in the distal airways and alveoli are mainly caused by the following

  • Irritating and toxic gases
  • Suspended soot particles
  • Vapors associated with incomplete combustion and smoke

Many of the substances found in smoke are extremely caustic to the tracheobronchial tree and poisonous to the body

The progression of injuries that develop from smoke inhalation and burns is described as the early stage, intermediate stage, and late stage

43
Q

Inhalation Injury Early Stage

(0 to 24 hours after inhalation)

A
  • Delayed onset of pulmonary symptoms, from none to marked presentation at 24 hours
    • Even when extensive body surface burns are evident!
44
Q

Inhalation Injury Early Stage

(0 to 24 hours after inhalation)

The tracheobronchial tree manifests with:

A
  • Inflammation
  • Bronchospasm
  • Increased bronchial secretions
    • Toxins can slow activity of the mucociliarytransport, further exacerbating secretion retention
    • Can lead to airway obstruction
45
Q

Inhalation Injury Early Stage

(0 to 24 hours after inhalation)

Other Complications

A
  • Non-cardiogenic Pulmonary Edema
    • Secondary to the inflammatory response and “leaky” AC membrane
    • May also be caused by overhydrationresulting from overzealous fluid resuscitation
    • In severe cases, acute respiratory distress syndrome (ARDS) also may occur early in the course of the pathology.
46
Q

Inhalation Injury Intermediate Stage

2 to 5 days after inhalation

A

Improvement/resolution ofupper airway thermal injuries

Peaking of the pathologic changesassociated with smoke inhalation deep in the lungs

47
Q

Inhalation Injury Intermediate Stage

Signs and Symptons

A

2 to 5 days after inhalation

–Mucous production continues to increase, while mucosal ciliarytransport activity continues to decrease

–The mucosa of the tracheobronchial tree frequently becomes necrotic and sloughs (usually at 3 to 4 days)

–The necrotic debris, excessive mucous production, and mucous retention lead to mucous plugging and atelectasis

–In addition, the mucous accumulation often leads to bacterial colonization, bronchitis, and pneumonia

48
Q

Imtermediate Stage

Other Complications

A
  • Pneumonia
    • Organisms commonly cultured include gram-positive Staphylococcus aureusand gram-negatives (Klebsiella, Enterobacter, Escherichia coli, Pseudomonas)
  • If not already present, ARDS may develop
  • When chest wall (thorax) burns are present:
    • Situation may be further aggravated by the patient’s inability to breathe deeply and cough (Pain, analgesics, immobility, poor lung mechanics…)
49
Q

Inhalaton Injury Late Stage

A

5 or More Days after Inhalation

Progression with concerns now focused on:

  • Infection
    • resulting from burn wounds on the body surface
    • These infections often lead to sepsis and multi-organ failure.
  • Pneumonia (still)
  • Pulmonary embolism (secondary to a hypercoagulablestate)

Sepsis-induced multi-organ failure is the primary cause of death in seriously burned patients during this stage.

50
Q

Inhalation Injury Late Stage

Long Term Concerns

A

Long-term effects of smoke inhalation can result in restrictive and obstructive lung disorders.

  • Restrictive lung disorder
    • Develops from alveolar fibrosis and chronic atelectasis.
  • Obstructive lung disorder
    • Generally is caused by increased and chronic bronchial secretions, bronchial stenosis, bronchial polyps, bronchiectasis, and bronchiolitis.
    • Cryptogenic organizing pneumonia (also called bronchiolitisobliteransorganizing pneumonia [BOOP])
51
Q

Inhalation Injury

Pathophysiological Mechanism

A

–Atelectasis

–Alveolar Consolidation

–Increased Alveolar-Capillary Membrane Thickness

–Bronchospasm

–Excessive Bronchial Secretions

52
Q

Inhalation Injury

Physical Examination

A
  • Vital Signs: Increased RR, HR, BP
  • Assessment of Upper Airway (Thermal Injury)
    • Obvious pharyngeal edema and swelling
    • Inspiratory stridor
    • Hoarseness; altered voiced
    • Painful swallowing
  • Other
    • Cyanosis
    • Cough and sputum production
  • Chest Assessment Findings
    • Usually normal breath sounds (early stage)
    • Wheezing, crackles, rhonchi
53
Q

Inhalation Injury

Clinical Data-ABGs

A
  • Early stage
    • Acute respiratory alkalosis with hypoxemia
  • Severe smoke inhalation and burns
    • Combined respiratory and metabolic (lactic) acidosis
    • PaO2 may be normal but tissue hypoxia 2°COHb
  • Late stage:
    • Acute respiratory acidosis
54
Q

Inhalation Injury

Chest Xray

A

–Usually normal (early stage)

–Pulmonary edema/ARDS (intermediate stage)

–Patchy or segmental infiltrate (late stage)

55
Q

Inhalation Injury

Oxygenation Indices-Late Stage

A
  • DO2
    • Decrease
  • VO2
    • Decrease
  • C(av)O2
    • Decrease
  • O2ER
    • Decrease
  • SvO2
    • Decrease
56
Q

Inhalation Injury

Hemodynamics-Late Stage

A

Hypovolemic initially; then more of a septic picture/SIRS with vasodilation

  • CVP
    • Decrease
  • PAP
    • Decrease
  • PAWP
    • Decrease
  • SV
    • Decrease
  • CO
    • Decrease
  • SVR
    • Increased
  • PVR
    • Increased
57
Q

Inhalation Injury

Hemodynamics-Early/ Intermediate Stage

A

Hypovolemic initially; then more of a septic picture/SIRS with vasodilation

  • CVP
    • Decrease
  • PAP
    • Decrease
  • PAWP
    • Decrease
  • SV
    • Decrease
  • CO
    • Decrease
  • SVR
    • Increased
  • PVR
    • Normal
58
Q

Inhalation Injury

Oxygenation Indices-Early/ Intermediate Stage

A
  • DO2
    • Decrease
  • VO2
    • Increase
  • C(av)O2
    • increase
  • O2ER
    • Increase
  • SvO2
    • Decrease
59
Q

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation

0-10% COHB

A

Usually no symptons

60
Q

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation

10-20% COHB

A

Mild Headache

Dilation of cutaneous blood vessels

61
Q

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation

20-30% COHB

A

Throbbing headache

Nausea

Vomitting

Impaired judgment

62
Q

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation

30-50% COHB

A

Throbbing headache, possible syncope,

Increased RR and HR

63
Q

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation

50-60% COHB

A

Syncope

Increased RR and HR

Coma

Convulsions

Cheyne-Stokes Respirations

64
Q

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation

60-70% COHB

A

Coma

Convulsion

Cardiovascular and Respiratory Depression

Possible Death

65
Q

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation

70-80% COHB

A

Cariopulmonary failure and death

66
Q

Inhalation Injury

Immediate Assessment

A

–*Airway and respiratory status

–Cardiovascular status

–The percentage of body burned

–Depth of burns

67
Q

Inhalation Injury

Fluid Resuscitation

A
  • IV access is a priority
  • Fluid resuscitation (based on a formula)
    • 4 mL/kg of body weight for each percent of body surface area burned over a 24-hour period.
  • The patient’s hemodynamic status will usually remain stable at this fluid replacement rate, with an average urine output target of 30 to 50 mL/hrand a central venous pressure (CVP) target of 2 to 6 mm Hg.
    • U/O 30—50 mL/Hr, CVP 2-6 mmHg

Because this process often leads to overhydrationand acute upper airway obstruction and pulmonary edema, the patient’s fluid and electrolyte status must be monitored carefully.

68
Q

Early Management

A

–Easily separated clothing should be removed.

–Any remaining clothing should be soaked thoroughly before removing.

–When present, burn wounds should be covered to prevent shock, fluid loss, heat loss, and pain.

–Infection control includes isolation, room pressurization, air filtration, and wound coverings. Wound care is a sterile procedure.

Knowledge of the exposure characteristics of the fire-related accident may be helpful in assessing the potential clinical complications

69
Q

General Management

A
  • Airway management—the elective endotracheal intubationshould be performed on the patient who has inhaled hot gases and demonstrates any signs of impending UAO (ie. Stridor)
  • Consider early intubation - Awake Intubation with fiberopticbronchoscopy
  • Heated Active Humidity –Treat hypothermia and thick secretions, mucous plugs and eschar
  • Bronchoscopy— therapeutic bronchoscopy is often used to clear the airway of mucous plugs and eschar.
  • Hyperbaric oxygen therapy—may be useful in the rapid elimination of CO and the enhancement of skin graft viability.
  • Treatment for cyanide poisoning—includes amyl nitrite inhalation and intravenous sodium thiosulfate
70
Q

General Management-Pharmacology

A
  • Antibiotic agents—may be used to treat burn wounds and pulmonary infections
  • Expectorants—may be administered to facilitate expectoration
  • Analgesic agents—are generally ordered when surface burns are present
  • Prophylactic anticoagulants—heparin and other anticoagulants often are administered to patients with severe, long-term fire-related injuries
71
Q

General Respiratory Care

A

–Oxygen Therapy

–Mechanical Ventilation

–Bronchopulmonary Hygiene

–Lung Expansion Therapy

–Aerosolized Medication

Pathophysiology 2 (9 decks)

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