Mechanical ventilation, sedation and analgesia in pediatric burns

49
Sergey Shushunov MD

Transcript of Mechanical ventilation, sedation and analgesia in pediatric burns

Page 1: Mechanical ventilation, sedation and analgesia in pediatric burns

Sergey Shushunov MD

Page 2: Mechanical ventilation, sedation and analgesia in pediatric burns

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%

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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

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Local

tissue injury, inflammation, infection

Systemic

Hemolysis, malnutrition, stress, immunodeficiency,

SIRS / MODS

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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

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Local inflammation, lymphatic and venous obstruction, edema, eschar formation

Neck - laryngeal obstruction Chest - decrease chest wall compliance

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Elevated air temperature Oxygen depletion Smoke generation

Carbon particles

Carbon monoxide

Cyanides

Chemicals irritants

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Leading cause of death in

burn patients

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Up to 80% of fire deaths occur at the scene Smoke inhalation effects

Asphyxiation

Thermal airway injury

Inhalation of chemical irritants

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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

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O₂ concentration <10% 10% O₂ in air = O₂ pp at 18,000 ft Affects judgment Affects mobility Negative synergism with CO and CN

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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

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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

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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

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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.

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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

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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

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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

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Increased bronchial secretions Bronchospasm Cast formation Obliterating bronchiolitis Small airway edema Depletion of surfactant Acute lung injury / ARDS Systemic effect due to absorption

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Greatly increases the occurrence of postburn morbidity and mortality

Immunosuppression, presence of ET tube and airway damage predispose to pneumonia

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O₂ Hyperbaric chamber with supplemental

oxygen when HbCO >25% Endotracheal intubation and MV for severely

depressed mental status is rarely required

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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

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Epinephrine aerosols Head elevation Heliox

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Injury above the cords (thermal) Injury below the cords (chemical) ARDS / pneumonia

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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

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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

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Frequent endotracheal lavage and suction Serial therapeutic bronchoscopies Albuterol and epinephrine aerosols DNA’s aerosols Heparin/acetylcysteine aerosols High humidity (no passive humidifiers)

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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

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Sedation for mechanical ventilation Analgesia for the injury Analgesia for debridement and dressing

changes

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Not intubated verbal child Not intubated non-verbal child Intubated child without NMB Intubated child with NMB

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Ventilator synchrony Airway protection Deep sedation is usually required

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PMH Previous experience with anesthesia / sedation Allergies Medications NPO status PE

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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

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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

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Drug Sedation AnalgesiaFentanyl + +++Morphine + +++Lorazepam ++ –Midazolam ++ –Pentobarbital +++ –Diprivan +++ –Dexmedetomidine ++ ++Ketamine +++ +++

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Morphine Fentanyl Oxycodone

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Diprivan Diprivan / fentanyl Ketamine Ketamine / midazolam Fentanyl or morphine Midazolam / fentanyl or morphine Midazolam / fentanyl / dexmedetomidine Fentanyl / dexmedetomidine

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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

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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

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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

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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

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