inhalation trauma, burn 2012

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EMERGENCY ASSESMENT & UPDATE

MANAGEMENT OF SEVERE BURN 2012

MALANG MEDICAL ASSO CIATION (MMA)

SEMINAR SE-JAWA BALI, on 1st April 2012


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INITIAL BURN MANAGEMENTFOCUS ON

INHALATION TRAUMA

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YUDDY IMOWANTO


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BURN EPIDEMIOLOGY

According to the ABA, 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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incidence

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BURN EPIDEMIOLOGY

The majority of burns occur from fire (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 vitalbody areas as the face, hands, and feet.

The overall survival rate from burns in the years 1995to 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

Upper airway injury that results in obstruction during thefirst 12 h after-insult is caused by direct thermal injury aswell as chemical irritation.

The second important factor in the pathophysiology ofinhalation injury is the marked decrease in pulmonarycompliance, which can be reduced by more than 50%.

In the first 24 h after-injury, this fall in the compliancecorresponds with increases in the extravascular lungwater and pulmonary lymph flow.

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Survivability of Burns

Most common cause of death is inhalation injury.

Increased risk of death:

Age > 60 years

burns > 40% TBSA

smoke inhalation injury

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At center of burn is a zone of irreversible coagulativenecrosis that is formed immediately after injury.

Surrounding this central core is a zone of ischemia in

which there is a reduction in the dermalmicrocirculation, putting this area at risk for subsequentnecrosis if the perfusion is not improved.

The third and outermost zone is the zone of hyperemia,

characterized by an immediate and transient increase inperfusion.



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Concerns related to burn injury

1. Early assess for airway compromise from inhalation injuryinhaled products can induce pulmonary parenchymal damageand further worsen the patients respiratory status.

2. Patients with > 20% TBSA burns are hypovolemic state.

3. Approx 10% of burn patients suffer concomitant injuries.A focused examination is important to determine the possibilityof neurologic or musculoskeletal injury.

4. Patient should be completely exposed to assess for the extentof burn, and for evidence of any associated trauma.



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important investigations

include:1. Arterial blood gas and pulse oximetry. Early detection ofhypoxia and/or hypercapnia in patients with inhalationinjury is documented by these tests.

2. Carboxyhemoglobin levels. Patients in closed-space firesare at risk for CO poisoning. CO has an affinity forhemoglobin 40 times that of oxygen and may falsely

elevate pulse oximetry readings.A carboxyhemoglobin level up to 10 may be normal forchronic smokers



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include:3. CXR. Though the initial chest radiographs may be normalin early inhalation injury, it may demonstrate parenchymalabnormalities such as pulmonary edema.

4. Flexible laryyngoscopy/bronchoscopy.

These procedures can be done at the bedside to furtherevaluate the airways of patients with suspected inhalation

injury. Visualization of airway erythema, edema,carbonaceous sputum, and singed nose hair all signifyinhalation injury.



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include:5. Doppler stethoscope. Extensive burns of the

extremities and subsequent edema make peripheral

pulses difficult to palpate, and Doppler stethoscopemay help detect weak pulses.

6. Compartment pressure measurement. A high index ofsuspicion should exist for compartment syndrome.

Whenever suspected, objective measurements can assist infurther clinical management.



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include:7. Serum glucose. Glycemic control can reduce osmoticdiuresis and infectious complications, and may improve

survival.

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 andoxides of sulfur and nitrogen.

Other toxic compounds released from burning ofcommon household materials such as

polyvinylchlorides include hydrochloric acid andcarbon 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 injuredtracheobronchial mucosa, with progressive shedding of

the necrotic lining of the airway and the formation ofpseudomembranous casts that partially or completelyobstruct the airway.

there may be severe edema and congestion of the

pulmonary parenchyma with infiltration of leukocytesthat release additional inflammatory mediators andreactive oxygen species that further contribute tobronchospasm, tissue inflammation, and destruction.

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Pathophysiology of

Inhalation Injury deactivation of pulmonary surfactant, leading to areas of

microatelectasis causing ventilation perfusion mismatchand pulmonary shunting, and results in progressivehypoxemia and

Once activated inflammatory cells are in the area ofinjury, they release a large number of inflammatory

mediators or cytokines as well as cytotoxic reactiveoxygen and nitrogen species, can cause clinical syndromeof acute respiratory distress syndrome.

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Recognizing Inhalation

Injury Smoke inhalation injury affects between 5 and 35% of

hospitalized burn patients.

With improvements in fluid resuscitation, inhalationinjury has become one of the two causes of morbidityand mortality in burn patients.

The presence of inhalation injury increases the

mortality from burns by 20% and when combined withpneumonia by 60%.

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Injury 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 highlyspecific.

wheezing, crepitations, hypoxemia, and abnormalities onthe initial CXR may or may not be present in the ED,except in the most severely injured.

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Injury diagnosis of inhalation injury in the ED is best made

by direct visualization of the airways with fiberopticlaryngoscopy (before intubation) and bronchoscopy (after

intubation).

Findings of inhalation injury include the presence ofsoot, charring, and mucosal inflammation, edema, ornecrosis.

While bronchoscopy is useful in identifying injury tothe airway, it cannot exclude parenchymal injury.


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Injury Diagnosis of injury to the parenchyma of the lung is best made

using xenon ventilation scanning, which demonstrates areas ofdecreased alveolar gas washout secondary to small airway

obstruction.

Carbon monoxide levels should be based on measurement ofserum carbon monoxide levels using co-oximetry.

Cyanide, a frequent combustion product of plastics, should be

suspected in patients in a closed space fire with elevatedcarbon 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 thesynthesis of inducible nitric oxide synthase, which leads to

further production of nitric oxide, an important reactivenitrogen species.

Reactive oxygen species results in damage to DNA, proteins,and lipids. Lipid peroxidation is thought to cause oxidativedamage to cellular membrane & eventually result in cell death

Reactive nitrogen species (nitric oxide) also inhibit T cells,thus participating in the immunosuppression associated withlarge 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 mustbe 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 atintubation 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 or a P


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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 managementmay contribute to an exaggerated inflammatory and

stress response, Inadequate analgesia may be due to the distraction of

the often dramatic burn wound or other associatedinjuries, 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 ofpain management

Procedural pain refers to the pain experienced when theburn wound is manipulated or dbrided.

Pain is generally very severe but transient in nature.

Adding anxiolytic medication to parenteral opioids isuseful during this phase of management.

Cooling of burns with cold water can significantly reducepain. The optimal cooling temperature is around 10 to25 C, which is approx. the temperature of tap water.

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PAIN MANAGEMENT

Moderate to severe burn pain is managed with parenteralopioids (morphine sulfate 0.050.1 mg/kg) titrated to effect

The intravenous route is recommended due to its rapid andreliable effects and consistent absorption.

Fentanyl 0.5 to 1.0 g/kg may be used for managingbreakthrough & procedural pain. Intranasal fentanyl at adose of 1.4 g/kg may be as effective as oral morphine inboth children and adults.

Intravenous infusion of lidocaine (1 mg/kg bolus followed by24 mg/min infusion) can reduce the severity of pain in burnpatients.

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Widened QRS complexes in a patient whose

serum potassium level was 7.8 mEq/L.

14/06/2013 39http://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.

14/06/2013 40http://emedicine.medscape.com/article/766479-workup#a0721

ll d i Z f ld ( i h f S d T )


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14/06/2013 41Tintinalli's Emergency Medicine 7th edition

called sine wave or Z-fold appearance (merging together of S-wave and T-wave)


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Inhalation Injury Above the Glottis

1. Upper airway

structures susceptible

to injury if exposed to

high temperatures

2. Signs and symptoms

3. Prehospital care



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Inhalation Injury Below the Glottis

Mechanisms of direct

injury to lung tissue

Heat (steam) Toxic material

inhalation

S/S often delayed Prehospital care

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Goals of Prehospital Burn

Management Preventing further tissue injury

Maintaining patent airway

Administering oxygen and ventilatory support Fluid resuscitation (per protocol)

Pain Control

Rapid transport to appropriate medical facility Psychological and emotional support



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Treatment-management

Airway

Assess for airway compromise

Assess for soot around face, singed facial/nasalhair, hoarseness, wheezing, cough, stridor orinability to swallow.

Secure/ Maintain airway

High FiO2 (15L NRB)


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Breathing

Assist with BVM if needed

If inhalation injury is suspected, closely observefor signs of impending airway obstruction:

Laryngeal edema may be progressive and maymake tracheal intubation difficult or impossible

Do not delay intubation in these patients



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Speaking of Fluid Resuscitation

Does that say Lactated Ringers instead ofNS??

4ml LR/.9NS x% TBSA burned x patients wt in kg

Example: TBSA burned 40%, Patient wt. 70kg

4ml x 40 x 70 = 11,200ml

in 1st 8hrs 5,600ml

in 2nd 8hrs 2,800ml

in 3rd 8hr

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Treatment

is based on aggressive fluid resuscitation to achieve aurine 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 preventmyoglobin 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 thedevelopment of extremity compartment syndrome.



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Conclusion

Inhalation injury and associated major burns provide

a challenge for health care workers who provide

direct hands-on care.

The technical and physiologic problems whichcomplicate the respiratory management of these

patients require an orderly, systematic approach.

Successful outcomes require careful attention totreatment priorities, protocols and meticulous

attention to details

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inhalation trauma, burn 2012

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