Burns and Inhalation Injuries Flashcards
Burns Definition
Injury or damage resulting from exposure to fire, heat, caustics, electricity, or certain radiations
Inhalation Injuries
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.
Smoke
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.
What Kind of Substance does wood, cottom and paper produce when they are burned
Aldehydes (acrolein, acetaldehyde, formaldehyde)
Organic Acids (acetic and formic acids)
What kind of substance does polyvinycloride produce when they are burned
Carbon Monixide
Hydrogran Chloride
Phosgene
What kind of substance does Polyurethanes produce when they are burned
Hydrogen Cyanide
What kind of substance does Flurinated Resins produce when they are burned
Hydrogen Fluride
Hydrogen Bromide
What kind of substance does Nitrocellulose Film and Fabrics produce when they are burned
Oxides of Nitrogen
What kind of substance does Melamine Resins produce when they are burned
Ammonia
What kind of substance does Petroleum Products produce when they are burned
Benzene
What kind of substance does Organic Material produce when they are burned
Carbon Monoxide
Carbon Dioxide
What kind of substance does Sulfur Continaing Compounds produce when they are burned
Sulfur Dioxide
What kind of substance does Fertiizer, Textiles, Rubber produce when they are burned
Hydrogen Chloride
What kind of substance does Swimming Pool Water produce when they are burned
Chlorine
What kind of substance does Welding Fumes produce when they are burned
Ozone
What kind of substance does Metal Works and Chemical Manufactuering produce when they are burned
Hydrogen Sulfide
The prognosis of fire victims usually is determined by
- Extent and duration of smoke exposure
- Chemical composition of the smoke
- Size and depth of body surface burns
- Temperature of gases inhaled
- Age (the prognosis worsens in the very young or old)
- Pre-existing health status
1st Degree Burns
Clinical Apperance
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
1st Degree Burns
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
2nd Degree Burns
Clinical Picture
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
2nd Degree Burns
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
Third Degree Burns
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
Third Degree Burns
Clinical Picture
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
Determination of Area - Surface Burns
For Infants
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
Determination of Area - Surface Burns
For Adults
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
Large 3rd Degree Burns Can Lead To
- 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
Burned Skin
Will lose it elasticity
Can impair local tissue perfusion
May cause tissue necrosis
If Circumferential Around the Thorax
Burns can decrease chest wall compliance“Third spacing”
Tissue Hypoxia
–inhalation of toxic gases
–inhalational burns,
–or from inadequate perfusion
Surface Burns and Cardiac Instability
Early- Decreased CO and Increased SVR
Later- Decreased SVR
Surface Burns and Metabolic Changes
Initial anaerobic metabolism
Develops a hypermetabolic state
Presents as Catabolic Hypermatabolism
Hypermetabolic State
Caused by massive catechoalmine release post butn
Can last up to 2 years post burn
Hypermetabolic State is Charaterized By
–Increased metabolic rates
–Multi-organ dysfunction
–Muscle protein degradation,
–Blunted growth,
–Insulin resistance
–Increased risk for infection
Catabolic Hypermetabolism
Pt begins to consume blood and muscle proteins
Surface Burns and Immune Function
Decreased immune function
Possible reduction in WBC formation
Surface Burns and CNS
Patients tend to reset thermo-homeostatic point (~38 degCelsius or higher) due to the hypermetabolic state
Surface Burns and Other Complications
–Risk of Pulmonary thromboembolism is high in later stages
–Infection, sepsis, and gangrene can all occur
–Multi-organ system failure & death
–ARDS
Anatomic Alterations of the Lungs
Thermal Injury
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!!
Anatomic Alteration of the Lungs Thermal Injury
Manifestations
Blistering
Mucosal edema
Vascular congestion
Epithelial sloughing
Thick secretions
Acute upper airway obstruction
Thermal Injuries and the Distal Airways
- 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.
Anatomic Alterations of the Lungs
Smoe Inhalation Injury
Tracheobronchial Tree and Alveoli
–Inflammation of the tracheobronchial tree
–Bronchospasm
–Excessive bronchial secretions and mucous plugging
–Decreased mucociliarytransport
–Atelectasis
Smoke Inhalation Injury
Pathological Changes
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
Inhalation Injury Early Stage
(0 to 24 hours after inhalation)
- Delayed onset of pulmonary symptoms, from none to marked presentation at 24 hours
- Even when extensive body surface burns are evident!
Inhalation Injury Early Stage
(0 to 24 hours after inhalation)
The tracheobronchial tree manifests with:
- Inflammation
- Bronchospasm
- Increased bronchial secretions
- Toxins can slow activity of the mucociliarytransport, further exacerbating secretion retention
- Can lead to airway obstruction
Inhalation Injury Early Stage
(0 to 24 hours after inhalation)
Other Complications
- 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.
Inhalation Injury Intermediate Stage
2 to 5 days after inhalation
Improvement/resolution ofupper airway thermal injuries
Peaking of the pathologic changesassociated with smoke inhalation deep in the lungs
Inhalation Injury Intermediate Stage
Signs and Symptons
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
Imtermediate Stage
Other Complications
- 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…)
Inhalaton Injury Late Stage
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.
Inhalation Injury Late Stage
Long Term Concerns
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])
Inhalation Injury
Pathophysiological Mechanism
–Atelectasis
–Alveolar Consolidation
–Increased Alveolar-Capillary Membrane Thickness
–Bronchospasm
–Excessive Bronchial Secretions
Inhalation Injury
Physical Examination
- 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
Inhalation Injury
Clinical Data-ABGs
- 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
Inhalation Injury
Chest Xray
–Usually normal (early stage)
–Pulmonary edema/ARDS (intermediate stage)
–Patchy or segmental infiltrate (late stage)
Inhalation Injury
Oxygenation Indices-Late Stage
- DO2
- Decrease
- VO2
- Decrease
- C(av)O2
- Decrease
- O2ER
- Decrease
- SvO2
- Decrease
Inhalation Injury
Hemodynamics-Late Stage
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
Inhalation Injury
Hemodynamics-Early/ Intermediate Stage
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
Inhalation Injury
Oxygenation Indices-Early/ Intermediate Stage
- DO2
- Decrease
- VO2
- Increase
- C(av)O2
- increase
- O2ER
- Increase
- SvO2
- Decrease
Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation
0-10% COHB
Usually no symptons
Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation
10-20% COHB
Mild Headache
Dilation of cutaneous blood vessels
Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation
20-30% COHB
Throbbing headache
Nausea
Vomitting
Impaired judgment
Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation
30-50% COHB
Throbbing headache, possible syncope,
Increased RR and HR
Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation
50-60% COHB
Syncope
Increased RR and HR
Coma
Convulsions
Cheyne-Stokes Respirations
Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation
60-70% COHB
Coma
Convulsion
Cardiovascular and Respiratory Depression
Possible Death
Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestation
70-80% COHB
Cariopulmonary failure and death
Inhalation Injury
Immediate Assessment
–*Airway and respiratory status
–Cardiovascular status
–The percentage of body burned
–Depth of burns
Inhalation Injury
Fluid Resuscitation
- 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.
Early Management
–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
General Management
- 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
General Management-Pharmacology
- 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
General Respiratory Care
–Oxygen Therapy
–Mechanical Ventilation
–Bronchopulmonary Hygiene
–Lung Expansion Therapy
–Aerosolized Medication
