Post on 16-Jul-2015
transcript
Sergey Shushunov MD
150,00 / year total; 60,000 / year <5 y/o Accidental / intentional Leading cause of death of children at home Mortality
Burns alone <2%
Smoke inhalation alone 7%
Burns & smoke inhalation 29%
Characteristic Number
Total admissions 1989-2009 5260Total number of deaths 145Mortality (%) 2.8Age of deceased (years) 7 ± 6Burn surface area of deceased (%) 69 ± 2Respiratory failure (%) 29Brain death (%) 16Shock (%) 8Sepsis (%) 47Inhalation injury among deceased (%) 71Time until death post-burn (days) 29 ± 50
Local
tissue injury, inflammation, infection
Systemic
Hemolysis, malnutrition, stress, immunodeficiency,
SIRS / MODS
Circumferential burns of neck and chest Smoke inhalation
asphyxiation toxyndromeupper airways thermal injurylower airways chemical injury
ARDS due to SIRS or lower airway injury Pneumonia
Local inflammation, lymphatic and venous obstruction, edema, eschar formation
Neck - laryngeal obstruction Chest - decrease chest wall compliance
Elevated air temperature Oxygen depletion Smoke generation
Carbon particles
Carbon monoxide
Cyanides
Chemicals irritants
Leading cause of death in
burn patients
Up to 80% of fire deaths occur at the scene Smoke inhalation effects
Asphyxiation
Thermal airway injury
Inhalation of chemical irritants
Probably the most common cause of fire death
Three components
O₂ depletion
Carbon monoxide (CO)
Cyanides (CN)
Combination of ↓O₂, CO and CN reduces time to death
O₂ concentration <10% 10% O₂ in air = O₂ pp at 18,000 ft Affects judgment Affects mobility Negative synergism with CO and CN
Released during combustion of any product Potentially lethal level 50%; LD50 = 60% Preferentially binds with the hemoglobin
molecule in place of oxygen Shifts the hemoglobin-oxygen dissociation
curve to the left, impairing oxygen unloading With heavy smoke the time to toxicity (CO
level 15-20%) is < 5 minutes
Recognized >30 years ago Results from incomplete combustion of
nitrogen containing materials One of the causes of death at the scene Sources of cyanide
Wool, silk Clothing, fabric, blankets, furniture
Polyurethane Insulation, upholstery
Polyacrylonitrile Appliances, engineering, plastics
Polyamide Carpeting, clothing
Polyamine resins Household and kitchen goods
Synthetic fire retardants
Found in at least 70% of fire burn victims Potentially lethal serum level 3.0 mg/L in
5-10% of victims Rapid absorption of HCN through the large
surface area of the lung Binds to the cytochrome system, leads to
tissue hypoxia Sustained loss of consciousness and CV
abnormalities Unexplained severe lactic acidosis
Signs and Symptoms CO CN
Headache + +
GI disturbances ++ +
Dizziness ++ +
Confusion ++ +
Seizures + +
Coma + +
Hypotension ++ ++
Cardiac arrhythmias ++ ++
Myocardial ischemia ++ ++
Loss of consciousness + +
Bradypnea - ++
clinical similarityreferred to as
asphyxiant toxidrome.
Rare below the vocal cords
effective heat dissipation in upper airways
laryngospasm
Airway edema evolves over 1-2 days May result from scalding burns SIRS may be a contributing factor
Oxygen radicals all burning productsMucus membrane damage, alveolar damage,systemic effect
Acrolein wood Mucus membrane damage, alveolar damage
Aldehydes wood, plastics Airway mucosa necrosis
Ammonia plastics Mucus membrane irritant
Sulfur dioxide rubber Mucus membrane irritant
Hydrogen chloride / phosgeneplastics, resins
Airway mucosa necrosis, alveolar damage
Benzenes wood, plastics Mucus membrane irritant, systemic toxins
Hydrogen sulfide rubberForms sulfuric acid, mucus membrane irritant and corrosive
Nitrogen dioxide fabrics, paperAlveolar damage, effect can be delayed by 72 hrs
Gaseous - quick onset (minutes-hours), shorter effect
Particulate – slower onset ( hours-days), longer effect, main contributor to the smoke inhalation lung injury
Fully evolves over a period of 3-5 days
Increased bronchial secretions Bronchospasm Cast formation Obliterating bronchiolitis Small airway edema Depletion of surfactant Acute lung injury / ARDS Systemic effect due to absorption
Greatly increases the occurrence of postburn morbidity and mortality
Immunosuppression, presence of ET tube and airway damage predispose to pneumonia
O₂ Hyperbaric chamber with supplemental
oxygen when HbCO >25% Endotracheal intubation and MV for severely
depressed mental status is rarely required
O₂ Antidotes
nitrates - form metHb; compete with binding to cytochromeoxidase; goal 25-40% of metHb
sodium thiosulfate - forms less toxic thiocyanate
dicobalt EDT - binds CN
hydroxocobalamin - binds CN, pseudohematuria
Endotracheal intubation and MV for severely depressed mental status
Epinephrine aerosols Head elevation Heliox
Injury above the cords (thermal) Injury below the cords (chemical) ARDS / pneumonia
Endotracheal intubation and MV to avoid loss of airways
Uncuffed ET tube Smaller than expected ET tube size Low settings, unless complicated by ARDS or
pneumonia: SIMV/CMV or VS/VC in older children, low PEEP, TV 8-10, low FiO₂
Sedation w/o or with NMB Brief duration (days)
Diagnostic bronchoscopy is recommended to r/o injury below the cords
Cuffed endotracheal tube Size as large as possible Settings determined by the changes in
compliance and airway resistance: SIMV/CMV,
variable PEEP, TV 4-10, high FiO₂, hypercarbia
Sedation with NMB Long duration (weeks)
HFPV, HFOV
Frequent endotracheal lavage and suction Serial therapeutic bronchoscopies Albuterol and epinephrine aerosols DNA’s aerosols Heparin/acetylcysteine aerosols High humidity (no passive humidifiers)
Cuffed endotracheal tube is preferred High settings: SIMV/CMV, high PEEP, TV 4-8, high FiO₂,
hypercarbia
Sedation with NMB Variable duration ( week/s)
HFOV NO Prone positioning
Sedation for mechanical ventilation Analgesia for the injury Analgesia for debridement and dressing
changes
Not intubated verbal child Not intubated non-verbal child Intubated child without NMB Intubated child with NMB
Ventilator synchrony Airway protection Deep sedation is usually required
PMH Previous experience with anesthesia / sedation Allergies Medications NPO status PE
ECG monitor Pulse oximeter BP monitor O2 source Suction Ventilation bag with correct size mask Nasal cannula Pediatric code cart / Intubation kit Drugs Reversing agents
Benzodiazepines: amnestic, anticonvulsant, anxiolytic,
sedative
Barbiturates: anticonvulsant, hypnotic, sedative
Diprivan: amnestic, hypnotic
Etomidate: amnestic, hypnotic
Dexmedetomidine: analgesic, anxiolytic, sedative
Chloral hydrate: hypnotic, sedative
Opioids: analgesic, sedative
Ketamine: analgesic, amnestic
Drug Sedation AnalgesiaFentanyl + +++Morphine + +++Lorazepam ++ –Midazolam ++ –Pentobarbital +++ –Diprivan +++ –Dexmedetomidine ++ ++Ketamine +++ +++
Morphine Fentanyl Oxycodone
Diprivan Diprivan / fentanyl Ketamine Ketamine / midazolam Fentanyl or morphine Midazolam / fentanyl or morphine Midazolam / fentanyl / dexmedetomidine Fentanyl / dexmedetomidine
Complication Management optionsAirway obstruction – Jaw thrust maneuver– Oro- or nasopharyngeal tube– Lateral positionApnea, hypopnea – Mask ventilation with supplemental oxygen– Intubation (if mask ventilation inadequate or not possible)Laryngospasm – Mask ventilation with supplemental oxygen– If severe: sedation, NMB and intubationVomiting – Lateral recumbent position, suctionAspiration – Supplemental oxygen – Intubation and MV– Bronchoscopy, chest radiograph if necessaryArterial hypotension – Volume replacement– In life-threatening cases: epinephrine IVBradycardia – Atropine IV– In life-threatening cases: IVAllergic reaction – Benadryl IV, ranitidine IV– Methylprednisolone IVAnaphylactic shock – Volume replacement, epinephrine IV
Described in children as young as 1 y/o Incidence in pediatric burns is about 30% ICU: sleep deprivation, threatening environment,
disrupted routine
Burn event and injury : pain, fear
Frequently unrecognized
Leads to psychiatric, circulatory, metabolic and immune system disorders
Long term physical, cognitive, emotional, behavioral and social problems
Lower severity and incidence in children treated with (larger doses) of morphine
Higher in children receiving benzodiazepines alone
Rogers’ Textbook of Pediatric Intensive Care 4th edition, David G. Nichols, editor . Lippincott Williams & Wilkins 2008
Rehberg S, Maybauer MO, Enkhbaatar P, Maybauer DM, Yamamoto Y, Traber Dl. Pathophysiology, management and treatment of smoke inhalation injury. Expert Rev Respir Med. 2009;3(3): 283–97.
P. Pervanidou, G. P. Chrousos. Post-traumatic Stress Disorder in Children and Adolescents:From Sigmund Freud's “Trauma” to Psychopathology and the (Dys)metabolic Syndrome.Horm Metab Res 2007; 39(6): 413-419
Meredith JR, O’KeefeKP, Galwankar S. Pediatric procedural sedation and analgesia. Emerg Trauma Shock. 2008:1(2)88-96
Williams FN, Herndon DN, Hawkins HK, Lee JO, Cox RA, Kulp GA, Finnerty CC, Chinkes DL, Jeschke MG. The leading causes of death after burn injury in a single pediatric burn center. Crit Care. 2009;13(6):R18