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INHALATION TRAUMA
Yuddy Imowanto
13/06/2013
BURN
EPIDEMIOLOGY
500,000 burn injuries are treated in medical facilities each year. This includes 4000 deaths, which occur mostly in residential fires. Of the 40,000 burn admissions/year, more than 60% are admitted to specialized burn centers.
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BURN
EPIDEMIOLOGY
scalds (32%), contact with hot objects (8%), electricity (4%), or chemical agents (3%). Over one third of admissions (38%) exceed 10% TBSA & 10% exceed 30% TBSA. Most admissions include severe burns of such vital body areas as the face, hands, and feet. The overall survival rate from burns in the years 1995 to 2005 was 94.4%.
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BURN
EPIDEMIOLOGY
indicates a decreasing trend in the number of burn visits from 1996 to 2000, with no further changes in trends from 2000 to 2005. Half of patients presenting to the ED were between the ages of 19 and 44 years.
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BURN
PATHOPHYSIOLOGY
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BURN
PATHOPHYSIOLOGY
coagulative necrosis that is formed immediately after injury. Surrounding this central core is a zone of ischemia in which there is a reduction in the dermal microcirculation, putting this area at risk for subsequent necrosis if the perfusion is not improved. The third and outermost zone is the zone of hyperemia, characterized by an immediate and transient increase in perfusion.
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thermal injury from steam or more commonly from the products of incomplete combustion such as the aldehydes and oxides of sulfur and nitrogen. Other toxic compounds released from burning of common household materials such as polyvinylchlorides include hydrochloric acid and carbon monoxide.
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to airway edema and deepithelialization of the injured tracheobronchial mucosa, with progressive shedding of the necrotic lining of the airway and the formation of pseudomembranous casts that partially or completely obstruct the airway. there may be severe edema and congestion of the pulmonary parenchyma with infiltration of leukocytes that release additional inflammatory mediators and reactive oxygen species that further contribute to bronchospasm, tissue inflammation, and destruction.
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microatelectasis causing ventilation perfusion mismatch and pulmonary shunting, and results in progressive hypoxemia and Once activated inflammatory cells are in the area of injury, they release a large number of inflammatory mediators or cytokines as well as cytotoxic reactive oxygen and nitrogen species, can cause clinical syndrome of acute respiratory distress syndrome.
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Recognizing Injury
Inhalation
hospitalized burn patients. With improvements in fluid resuscitation, inhalation injury has become one of the two causes of morbidity and mortality in burn patients. The presence of inhalation injury increases the mortality from burns by 20% and when combined with pneumonia by 60%.
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Recognizing Injury
Inhalation
findings such as facial burns, singed nasal vibrissae, carbonaceous sputum, and a history of injury within a closed space. These findings are neither highly sensitive nor highly specific. wheezing, crepitations, hypoxemia, and abnormalities on the initial CXR may or may not be present in the ED, except in the most severely injured.
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Recognizing Injury
Inhalation
by direct visualization of the airways with fiberoptic laryngoscopy (before intubation) and bronchoscopy (after intubation). Findings of inhalation injury include the presence of soot, charring, and mucosal inflammation, edema, or necrosis. While bronchoscopy is useful in identifying injury to the airway, it cannot exclude parenchymal injury.
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Recognizing Injury
Inhalation
made using xenon ventilation scanning, which demonstrates areas of decreased alveolar gas washout secondary to small airway obstruction. Carbon monoxide levels should be based on measurement of serum carbon monoxide levels using co-oximetry. Cyanide, a frequent combustion product of plastics, should be suspected in patients in a closed space fire with elevated carbon monoxide and elevated lactate levels.
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Inhalation injury. (A) Facial burn with singed facial hair in a man involved in a carfire. High suspicion for inhalation injury. This patient should undergo bronchoscopy. (C) The laryngotracheal view of inhalation injury at autopsy. Note the extensive erythema and carbonaceous materials throughout the airway.
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activate nuclear factor kappa beta, which induces the synthesis of inducible nitric oxide synthase, which leads to further production of nitric oxide, an important reactive nitrogen species. Reactive oxygen species results in damage to DNA, proteins, and lipids. Lipid peroxidation is thought to cause oxidative damage to cellular membrane & eventually result in cell death Reactive nitrogen species (nitric oxide) also inhibit T cells, thus participating in the immunosuppression associated with large burns
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(B) CXR demonstrating noncardiogenic pulmonary edema in a patient with severe inhalation injury.
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must be identified and addressed. If there is doubt regarding the presence of upper airway compromise, fiberoptic laryngoscopy should be performed. Endotracheal intubation guided by fiberoptic laryngoscopy is a useful technique, and if attempts at intubation are unsuccessful, surgical cricothyrotomy or needle cricothyrotomy may be necessary.
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Rule of Nines
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Burn Resuscitation
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An absolute compartment pressure >30mm Hg o r a P< 30 mmHg (MAP- compartment pressure) mandates escharotomy.
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escharotomy
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escharotomy
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PAIN
MANAGEMENT
Burns are among the most painful injuries. to being inhumane, inadequate pain management may contribute to an exaggerated inflammatory and stress response, Inadequate analgesia may be due to the distraction
of the often dramatic burn wound or other associated injuries, or concern that potent analgesics may impair ventilation. Pain management should be of primary concern for all burn patients.
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PAIN
MANAGEMENT
pain management Procedural pain refers to the pain experienced when the burn wound is manipulated or dbrided. Pain is generally very severe but transient in nature. Adding anxiolytic medication to parenteral opioids is useful during this phase of management. Cooling of burns with cold water can significantly reduce pain. The optimal cooling temperature is around 10 to 25 C, which is approx. the temperature of tap water.
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PAIN
MANAGEMENT
opioids (morphine sulfate 0.050.1 mg/kg) titrated to effect The intravenous route is recommended due to its rapid and reliable effects and consistent absorption. Fentanyl 0.5 to 1.0 g/kg may be used for managing breakthrough & procedural pain. Intranasal fentanyl at a dose of 1.4 g/kg may be as effective as oral morphine in both children and adults. Intravenous infusion of lidocaine (1 mg/kg bolus followed by 24 mg/min infusion) can reduce the severity of pain in burn patients.
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ECG-HyperKalemia
http://3.bp.blogspot.com/_2MjIeQJj8UM/S1fCR04mLUI/AAAAAAAABQM/o6eK8SiFq8w/s1600-h/rhythm_challenge_002_Cwm.JPG 13/06/2013
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http://emedicine.medscape.com/article/766479-workup#a0721
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Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.
http://emedicine.medscape.com/article/766479-workup#a0721
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ECG of a patient with pretreatment [K] level of 7.8 mEq/L & widened QRS complexes after receiving 1 amp of calcium chloride. Notice narrowing of QRS complexes and reduction of T waves.
http://emedicine.medscape.com/article/766479-workup#a0721
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called sine wave or Z-fold appearance (merging together of S-wave and T-wave)
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Treatment
is based on aggressive fluid resuscitation to achieve a
urine output of 1 cc/kg per hour. Other unproven but commonly practiced treatments include the use of mannitol to induce an osmotic diuresis, and urine alkalinization with bicarbonate to prevent myoglobin precipitation in the renal tubules. Patients should be monitored for a min of 6 hours, and often up to 24 hours, for cardiac arrhythmias and the development of extremity compartment syndrome.
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THANK YOU
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