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EMERGENCY ASSESMENT & UPDATE MANAGEMENT OF SEVERE BURN.

INHALATION TRAUMA
Yuddy Imowanto

13/06/2013

BURN

EPIDEMIOLOGY

According to the American Burn Association,

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

The majority of burns occur from fire/flame (46%),

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

The National Center for Health Statistics

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

At the center of burn is a zone of irreversible

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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Concerns related to burn injury


1. Early assess for airway compromise from inhalation injury inhaled products can induce pulmonary parenchymal damage and further worsen the patients respiratory status. 2. Patients with > 20% TBSA burns are hypovolemic from the predictable wound evaporative fluid loss and transudation of fluids into the extracellular space. 3. Approx 10% of burn patients suffer concomitant injuries. A focused examination is important to determine the possibility of neurologic or musculoskeletal injury. 4. Patient should be completely exposed to assess for the extent of burn, and for evidence of any associated trauma.

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important investigations include:


1. Arterial blood gas and puls e oximetry. Early detection of hypoxia and/or hyper capnia in patients with inhalation injury is documented by these tests. 2. Carboxyhemoglobin levels. Patients in closed-space fires are at risk for CO poisoning. CO has an affinity for hemoglobin 40 times that of oxygen and may falsely elevate pulse oximetry readings. A carboxyhemoglobin level up to 10 may be normal for chronic smokers
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important investigations include:


3. CXR. Though the initial chest radiographs may be normal in early inhalation injury, it may demonstrate parenchymal abnormalities such as pulmonary edema. 4. Flexible laryyngoscopy/bronchoscopy. These procedures can be done at the bedside to further evaluate the airways of patients with suspected inhalation injury. Visualization of airway erythema, edema, carbonaceous sputum, and singed nose hair all signify inhalation injury.

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important investigations include:


5. Doppler stethoscope. Extensive burns of the extremities and subsequent edema make peripheral pulses difficult to palpate, and Doppler stethoscope may help detect weak pulses. 6. Compartment pressure measurement. A high index of suspicion should exist for compartment syndrome. Whenever suspected, objective measurements can assist in further clinical management.
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important investigations include:


7. Serum glucose. Glycemic control can reduce osmotic diuresis and infectious complications, and may improve survival. Although, the precise target range is yet to be defined, most practitioners attempt to keep glucose below 180 mg/dL

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Pathophysiology of Inhalation Injury


Injury to the airways can be the direct result of

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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Pathophysiology of Inhalation Injury


Upper airway obstruction that occurs within the first few hours after injury is generally caused by chemical irritation. In up to one third of burn patients with inhalation injury, acute upper airway obstruction occurs due to the rapid progression of pharyngeal and supraglottic edema.

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Pathophysiology of Inhalation Injury


The upper and lower airway pathology is secondary

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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Pathophysiology of Inhalation Injury


deactivation of pulmonary surfactant, leading to areas of

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

Smoke inhalation injury affects between 5 and 35% of

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

inhalation injury was diagnosed based on clinical

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

diagnosis of inhalation injury in the ED is best made

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

Diagnosis of injury to the parenchyma of the lung is best

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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Pathophysiology of Inhalation Injury


The cytokines released(TNF alpha, [IL 1], and endotoxin)

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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EMERGENCY DEPARTMENT MANAGEMENT OF BURNS


focusing on the ABCs first. associated traumatic injuries or comorbidities that

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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Management of Inhalation Injury

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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

This chapter will only focus on the emergent phase of

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

Moderate to severe burn pain is managed with parenteral

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

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Widened QRS complexes in hyperkalemia.

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.

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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.

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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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