LIFE IN THE ICU:THERMAL INJURIESShawna Strickland PhD RRT-NPS RRT-ACCS AE-C FAARCAmerican Association for Respiratory Care

Disclosures• Employee,

American Association for Respiratory Care

• Adjunct Faculty, Rush University College of Health Sciences

• Any use of brand names is not in any way meant to be an endorsement of a specific product, but to merely illustrate a point of emphasis.

Objectives• Define anatomic changes, both pulmonary and systemic,

with burn injuries• Recognize signs and symptoms of patients with burn

injuries• Identify secondary pathological disease processes

associated with burn injuries• Discuss appropriate therapies for the pulmonary

management of patients with burn injuries• Decide, based upon clinical evidence, the best method of

ventilation for the patient with burn injuries

Case Study• 21 year old male suffered second- and third-degree burns

on his face, chest and abdomen as a result of his bed catching fire (TBSA 8%).

• After admission, he developed respiratory distress and pulmonary edema.

Physical Examination• Vital signs:

• BP 110/60 mm Hg• Pulse 100/min• RR 30/min• Temp 98.8°F• Breath Sounds:

• Bilateral crackles, rhonchi and wheezes

• Sputum:• Large amount thick,

whitish-grey sputum

• CXR:• Bilateral patchy infiltrates

and consolidation• ABG:

• pH: 7.51• PaCO2: 28 mm Hg• PaO2: 45 mm Hg• HCO3: 21 mEq/L

48 hours later…• Patient treated conservatively

(air entrainment mask at 50% oxygen)• Pulmonary edema cleared• Respiratory distress persisted• Bronchoscopy revealed extensive thermal damage to the

trachea and mainstem bronchi.• What would you do now?

Statistics and Definitions• ~1 million burn injuries occur each year

• This results in ~40,000 hospital admissions• Burn injuries receiving medical treatment: 486,000 • Fire/smoke inhalation deaths: 3,275• Male = 68%; Female = 32%

• Body surface burns• Burned area noted as TBSA (total body surface area) in

percentages• Inhalation injury

• Occurs in ~7-20% of burn admissions• Smoke inhalation

• Not just burning wood…• Hot gas inhalation

• Dry and steam…

59% Caucasian20% African-American14% Hispanic7% Other

Total Body Surface Area

Table 43-2. From Des Jardins & Burton (2006)

Lund-Browder Chart for Burn Assessment

Epidemiology of Burns• Accidental burns

• House fires, automobile accidents, farming accidents• Intentional burns

• Self-inflicted burns (predominantly suicide attempts)• Assault burns

• Place of occurrence:• Home: 73% • Occupational: 8% • Street/highway: 5% • Recreation/sport: 5%• Other: 9%

Etiology of Burns• Exposure to fire

• Most injuries occur in residential fires

• Exposure to superheated gases

• Exposure to scalding liquids• Scald burn most common thermal

injury in children

• Exposure to chemicals• Exposure to electrical currents

Recognition: Surface Burns• First degree: superficial; outer layer of

epidermis • Second degree: epidermal and dermal

involvement • Third degree: epidermis and dermis are

destroyed; damage extends to underlying tissues

• Fourth-degree burns: involve the tissues beneath the deepest layers of the skin, including muscles, tendons and even bones.

Respiratory Issues with Surface Burns• Patient is unable to breathe deeply and/or cough due to:• Increased pain• Use of narcotics• Immobility• Increased airway resistance• Decreased lung compliance• Decreased chest wall compliance

• Burned (tight) skin can impede the movement of the chest

Recognition: Inhalation Injuries• Hot Gas Inhalation

• Blistering of airway• Mucosal edema• Vascular congestion• Epithelial sloughing• Accumulation of thick

secretions• Upper airway obstruction

(20-30% of patients)

Recognition: Inhalation Injuries• Smoke Inhalation

• Early stage (0-24 hrs)• Inflamed tracheobronchial tree• Increased secretions• Slowing down of cilia• Pulmonary edema

• Intermediate stage (2-5 days)• Airway thermal injuries improve• Mucus production continues to increase• Sloughing of tracheobronchial mucosa (about day 3)• Pulmonary edema (if not already present) & ARDS

• Late stage (>5 days)• Infections are a major problem of this stage• Long-term effects: restrictive (fibrosis) and obstructive

(bronchiectasis/bronchiolitis) diseases

Smoke Inhalation and Thermal Injuries to the Airways

• Thick secretions

• Airway blister

• Mucosal edema

• Smoke (toxic gas)

• Frothy white secretions

Inhaled Toxins• Carbon Monoxide

• Hemoglobin loves CO…• CO can also bind to proteins containing heme• Results: fatigue, dysrhythmias, heart failure, seizures

and coma• Hydrogen Cyanide

• Easily transported to tissues • Does not allow oxygen/carbon dioxide exchange• Results: anaerobic metabolism and lactic acid

Clinical Appearance• respiratory rate• heart rate, cardiac output, blood pressure• Cyanosis• Stridor, hoarseness, altered voice• Painful swallowing• Breath sounds: wheezing, crackles, rhonchi

Hemodynamic Changes• DO2: lowered• VO2: initially increased, then drops• C(a-v)O2: initially increased, then drops• O2ER: initially increased, then drops• SvO2: lowered

Laboratory Values• Pulmonary functions:

• lung volumes/capacities/DLCO

• ABG:• Early: respiratory alkalosis with hypoxemia• Severe: metabolic (lactic) acidosis, normal oxygenation

(with tissue hypoxia), increased COHb

Table 43-3. From Des Jardins & Burton (2006)

Oxyhemoglobin Dissociation Curve

Radiographic Imaging: CXR• Early stage:

• normal • maybe pulmonary edema

• Intermediate stage: • pulmonary edema• ARDS

• Late stage:• Patchy or segmental infiltrates

72 hours Initial Injury Post-Injury

42 year old with phosgene inhalation

36 year old with chlorine

inhalation

Secondary Processes• VAP • ALI from transfusions (TRALI)• Abdominal compartment syndrome• Pneumonia (nosocomial)

• P. aeruginosa (associated with high mortality rate)• Staphylococcus aureus• Streptococcus pneumoniae• H. influenzae• MRSA

• Acute Stroke

Burn Edema• Caused by increased perfusion to injured area• Forms rapidly after injury

• 90% in the first four hours• Edema occurs in the dermis with superficial burns • With deep burns, edema resides in subcutaneous tissue

(because skin is destroyed)• Delayed resorption of fluid

Pharmacologic Treatment• Blood transfusions• Antibiotics• Corticosteroids• Analgesics• Nutritional support• Prophylactic anticoagulants

Fluid Resuscitation• Purpose:

• Burn shock is related to fluid loss• How to avoid burn shock? Give fluid!

• Problems:• How much fluid should be used?

• Many different formulas = confusion• Under-resuscitation• Over-resuscitation

• Fluids used: crystalloid, hypertonic, colloid

Respiratory Therapies• Airway management

• Intubate early for airway support• Burned (tight) skin can prevent you from opening the

airway• Bronchoscopy

• Can be used to grade the amount of injury• Hyperbaric oxygen• Inhaled nitric oxide

• Improves V/Q mismatch and oxygenation• Inhaled heparin and N-acetylcysteine

• Attenuates lung edema and cast formation

Problems with Ventilating the Burn Patient• Airway obstructions (increased resistance)• Development of pneumonia• Plugging of airways with secretions/tissue

• Leads to atelectasis• Fluid administration leaks into lung

• This results in a need for higher ventilator pressures resulting in baro- or volutrauma.

• Surface burns compromise compliance• Escharotomy may be necessary

Escharotomy

When: In the case of circumferential full thickness burns of the limbs and chest (don’t wait for compartment syndrome to show up first!)

Why: Relieve pressure placed on the body in that area-improve pulses or allow for improved chest rise by improving chest wall compliance

What: Incision to release pressure caused by fluid

Ventilator Management: General Factors• Non-invasive

• Not used much due to the need for an artificial airway• High VT and high PAP worsen mortality in those patients who develop ARDS.

• Adequate humidification (warm rooms)• Air trapping and Auto-PEEP• Treat like ARDS or COPD

• Depends on disease stage

Ventilator Management:Conventional Ventilation

• PC-CMV-CT or VC-CMV-CT?• Low compliance and high airway resistance can lead you

to be more aggressive…be careful!• Using a lung protective strategy (low VT, higher rates) is

most beneficial• One study supports high VT strategy (decreased vent days)

• Do you have CO poisoning?• Use 100% oxygen

No consensus at this time or evidence regarding “best” ventilator strategy to improve the number of ventilator-free days at 28 days.

Ventilator Management:Non-Conventional Ventilation• HFOV and HFPV…which one is better?

• High frequency percussive ventilation (VDR)• Showed improved outcome when burn was TSBA 40% or lower (not for

higher TBSA%)

• HFOV still shows some benefit• APRV

• Phigh at desired MAP• Plow at zero (reduce expiratory impedance)• Thigh: 5-6 seconds (increase MAP)• Tlow: 0.7-1 second (minimize de-recruitment)

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How children respond differently• Airway access is more difficult to obtain

• Will develop significant obstructions faster• Mild risk for cardiac dysfunction• Higher metabolic rate and need for nutrition• Difficult to assess neurologic function/pain levels in young children

• Thinner skin = deeper burns than adult

How the elderly respond differently• Reduced pulmonary function due to age

• Little pulmonary reserve; muscle weakness• Possible pre-existing coronary artery or valvular disease

• Nutrition complicated by endocrine problems or underlying malnutrition

• Baseline organic brain dysfunction may make pain levels difficult to assess

• Thin skin, compromised healing, graft may not heal

Prognosis• Morbidity/Mortality

• Currently: 5-10% for those that require hospitalization

• With increasing TBSA burns and age, mortality rates increase

• 80% TBSA and treated at burn center: 50% mortality

• Combat burn mortality:• 52% if TBSA is >50%

• Pre-existing conditions = poor prognosis• HIV/AIDS• Cardiac arrhythmias• Liver disease• Renal disease• CHF• Obesity • Alcohol abuse

Outcome of smoke inhalation injury based on exposure type

Finishing up the case…• Intubated

• Mechanical ventilation: • VC-CMV-CT (FiO2 0.50)

• IV steroids• CPT and postural drainage contraindicated due to chest burns

• In-line ultrasonic neb (bland aerosol) and suctioning for secretion control

12 days after intubation…• Patient’s vital signs and ABGs improved• Weaned to room air and extubated on day 12• Patient complained of exertional dyspnea but no dyspnea at rest

• Vital signs stables, breath sounds: crackles• CXR: flattened diaphragms, bilateral course reticular infiltrates

• ABG: normal with moderate hypoxemia

Case Conclusion• Over the next 6 weeks, the patient continued to have emphysematous changes on CXR.

• Aggressive cardiopulmonary therapy initiated• Patient expired on day 56 post injury.• Autopsy diagnosed bronchiolitis fibrosa obliterans

Case resource: Des Jardins & Burton

References• American Burn Association. Burn Incidence and Treatment in the United States:

2016.• Brusselaers N, Monstrey S, Snoeij T, Vandijck D, Lizy C, Hoste E, et al. Morbidity

and mortality of bloodstream infections in patients with severe burn injury. Am J Crit Care 2010;19 (6):e81-87.

• Chung KK, Wolf SE, Renz EM, Allan PF, Aden JK, Merrill GA, et al. High-frequency percussive ventilation and low tidal volume ventilation in burns: a randomized controlled trial. Crit Care Med 2010:38(10):1970-1977.

• Chung KK, Blackbourne LH, Wolf SE, White CE, Renz EM, Cancio LC, et al. Evolution of burn resuscitation in operation Iraqi Freedom. J Burn Care Res 2006;27(5):606-611.

• Des Jardins T, Burton, GC. Clinical manifestations and assessment of respiratory disease, 5th ed. St. Louis: Mosby; 2006.

• Eckert MJ, Wade TE, Davis KA, Luchette FA, Esposito TJ, Poulakidas SJ, et al. Ventilator-associated pneumonia after combined burn and trauma is caused by associated injuries and not the burn wound. J Burn Care Res 2006;27(4):457-462.

• Edelman DA, White MT, Tyburski GT, Wilson RF. Factors affecting prognosis of inhalation injury. J Burn Care Res 2006;27(6):848-853.

• Endorf FW, Gamelli RL. Inhalation injury, pulmonary perturbations, and fluid resuscitation. J Burn Care Res 2007;28(1):80-83.

• Greenlaugh DG. Burn resuscitation. J Burn Care Res 2007;28(4):555-565.

References• Hall JJ, Hunt JL, Arnoldo BD, Purdue GF. Use of high-frequency percussive

ventilation in inhalation injuries. J Burn Care Res 2007;28(3):396-400.• Hess DR, MacIntyre NR, Mishoe SC, Galvin WF, Adams AB, Saposnick AB.

Respiratory care principles & practices. Philadelphia: W.B. Saunders Company; 2002.

• Hicks GH, Eckrode, CA. Smoke inhalation injury and burns. In: Wilkins RL, Dexter JR, Gold PM. Respiratory disease: A case study approach to patient care, 3rd ed. Philadelphia: FA Davis; 2007.

• Higgins S, Fowler R. Callum J, Cartotto R. Transfusion-related acute lung injury in patients with burns. J Burns Care Res 2007;28(1):56-64.

• Ipaktchi K, Arbabi S. Advances in burn critical care. Crit Care Med 2006;34(9 Suppl):S239-S244.

• Jeschke MG, Herndon DN. Blood transfusion in burns: Benefit or risk? Crit Care Med 2006;34(6):1822-1833.

• Kacmarek RM, Dimas S, Mack CW. The essentials of respiratory care, 4th ed. St. Louis: Mosby; 2005.

• Lavrentieva A. Critical care of burn patients. New approaches to old problems. Burns 2016;42:13-19.

• Lee KC, Joory K, Moiemen. History of burns: the past, present and the future. Burns Trauma 2014;2(4):169-180.

• Mosier MJ, Peter T, Gamelli RL. Need for mechanical ventilation in pediatric scald burns: why it happens and why it matters. J Burn Care Res 2016;37:e1-e6.

References• Palazzo S, James-Veldsman E, Wall C, Hayes M, Vizcaychipi. Ventilation strategies in burn

intensive care: a retrospective observational study. Burns Trauma 2014;2(1):29-35.• Reiland A, Hovater M, McGwin G, Rue LW, Cross JM. The epidemiology of intentional burns.

J Burn Care Res 2006;27(3):276-280.• Saffle JR. The phenomenon of “fluid creep” in acute burn resuscitation. J Burn Care Res

2007;28(3):382-395.• Segu S, Tataria R. Paediatric suicidal burns: a growing concern. Burns, 2016: paper in

press.• Sheridan R. Burns at the extremities of age. J Burn Care Res 2007;28(4):580-585.• Sousse LE, Herndon DN, Andersen CR, Ali A, Benjamin NC, Granchi T, et al. High tidal

volume decreases adult respiratory distress syndrome, atelectasis, and ventilator days compared with low tidal volume in pediatric burned patients with inhalation injury. J Am CollSurg 2015;220(4):570-578.

• Starnes-Roubaud M, Bales EA, Williams-Resnick A, Lumb PD, Escuerdo JA, Chan LS, Garner WL. High frequency percussive ventilation and low FiO2. Burns 2012;38:984-99.

• Thombs BD, Singh VA, Halonen J, Diallo A, Milner SM. The effects of preexisting medical comorbidities on mortality and length of hospital stay in acute burn injury. Annals of Surgery 2007;245(4):629-634.

• Toon MH, Maybauer MO, Greenwood JE, Maybauer DM, Fraser JF. Management of acute smoke inhalation injury. Crit Care Resus 2010;12(1):53-61.

Thank you!Shawna Strickland PhD RRT-NPS RRT-ACCS AE-C FAARCAssociate Executive DirectorAmerican Association for Respiratory Care9425 N. MacArthur Blvd, Suite 100Irving, TX 75063

(972) 243-2272

shawna.strickland@aarc.org

@aarc_shawna