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Problem 2 – Emergency

Medicine
Gabriella Handayani
405130103
Burn depth classification
Depth Appearance Surface Sensation Time to healing
1st degree Epidermis Pink or red Dry Painful Days
2nd degree
(partial-
thickness) Epidermis + pars Pink, clear Moist Painful 14-21 days
-Superficial papilare blister

Epidermis + pars Pink, Moist Painful Weeks, or may


-Deep retikulare hemorrhagic progress to 3rd
blister, red degree, require
graft
3rd degree Epidermis + White, brown Dry Insensate Require excision
(full-thickness) dermis
4th degree Skin, subcutaneos Brown, Dry Insensate Require excision
fat, muscle, bone charred

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.809


• Injection of radioactive isotopes
and vital dyes, thermography,
photometry, nuclear imaging, and
ultrasound have been used to help
determine burn depth and predict
the potential of burns to heal.
• Currently the most promising tool
is laser Doppler imaging;however,
even this tool has little predictive
value in the early stages in the ED.

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.810


RULE OF NINE dr Wallace
Burn Severity

http://emcrit.org/030-064/056-thermal.burn.htm
Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.811
Treatment
Pre Hospital
• Stop the burning process, remove smoldering
clothes/jewelry.
• Establish patent airway; frequent reassessment:
– Intubate early for signs of respiratory distress.
• Initiate early IV fluid therapy.
• Relieve pain.
• Protect the wound with clean sheets.
• Transport to burn center (for major burns) if transport
time shorter than 30 minutes.
• Immobilize spine if decreased sensorium or trauma.

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.811


EMERGENCY DEPARTMENT
MANAGEMENT OF BURNS
• Airway Management  Endotracheal intubation
• General Measures for Moderate to Severe Burns
 intravenous access
• Circulation and Fluid Resuscitation  Fluid
resuscitation
• recognizing Inhalation Injury (soot, charring, and
mucosal inflammation, edema, or necrosis) 
endotracheal intubation and mechanical
ventilation
Treatment of the burn wound
• Silver sulfadiazine
• Mafedine acetate
• Silver nitrate
• Nearly healed: bacitracin, neomycin,
polymyxin B
Indications for Endotracheal Intubation and
Mechanical Ventilation
Upper airway obstruction
Inability to handle secretions
Hypoxemia despite 100% O2
Patient obtundation
Muscle fatigue suggested by a high or low respiratory rate

Hypoventilation (a Pco2 > 50 mm Hg and a pH less than


7.2)

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.812


Recommended Initial Ventilator Settings
Tidal volume 6–8 mL/kg
Respirator rate :
8–12 in adults
12–45 in children
Plateau pressures <35 cm H2O
I/E ratio 1 : 1–1 : 3
Flow rates 40–100 L/min
Flow rates 40–100 L/min
PEEP 8 cm H2O

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.812


Burn Resucitation Formula
FORMULA FIRST 24 FORMULA FIRST 24 HOURS FORMULA FIRST 24 HOURS
HOURS NEXT 24 NEXT 24 HOURS NEXT 24 HOURS
HOURS
Parkland LR 4 mL/kg/% burn within first 8 Colloids in amount of 20–
hr 60% of plasma volume;
glucose in water added to
maintain urine output
0.5–1.0 mL/kg/hr in adults
and 1 mL/kg/hr in children
Modified Parkland LR 4 mL/kg/% burn in adults Colloid infusion of 5%
albumin at the amount
(0.3–1 mL/kg/% burn)/16
per hr
Evans Crystalloids in the amount of 1 Crystalloids at 0.5 mL/kg/%
mL/kg/% burn, plus burn, colloids at
colloids at 1 mL/kg/% burn, plus 0.5 mL/kg/% burn, and the
2000 mL glucose same amount of glucose in
in water water as first 24 hr

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.813


Brooke LR 1.5 mL/kg/% burn, plus colloids at 0.5 LR 0.5 mL/kg/% burn,
mL/kg/% colloids at 0.25 mL/kg/%
burn, plus 2000 mL glucose in water burn,
and the same amount of
glucose in water as first 24
hr
Modified Modified Brooke LR 2 mL/kg/% burn in the Colloids 0.3–0.5 mL/kg/%
Brooke adult and 3 mL/kg/% burn, glucose in water to
burn in children maintain urine output
Monafo Solution containing 250 mEq Na, 150 mEq Solution titrated with 1/3
lactate, NS according to urine
100 mEq Cl; amount adjusted to urine output
output
Galveston LR at 5000 mL/m2 TBSA burned plus 2000 3750 mL/m2 TBSA burned
mL/m2 plus 1500 mL/m2 TBSA
TBSA, within 8 hr

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.813


Burn Dressings
• protect the wound, to reduce pain, to absorb
wound exudate, and, finally, to reduce vaporative
heat loss
• first-degree burns is not required other than
optional topical anesthetics, aloe vera, and/or
topical (NSAIDs).
• second-degree burns:
– the open method, which consists of topical
antimicrobials
– the closed method, which uses synthetic occlusive
dressings

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.815


Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.815
Escharotomy
• Releasing the constriction of a burn eschar
with a scalpel or cautery at the bedside
• The procedure is performed by making a
longitudinal incision down to the fat in the
constricting eschar
• Circumferential burn eschar may lead to
neurovascular compromise:
– Monitor pulses; may need Doppler flow probe.
– Elevate burned extremity.

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.816


Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.816
Electrical Burns
• Cellular Damage Due To Electrical Current High vs.
Low Tension Injuries
AC & DC
• High-voltage direct current (DC) :
– single muscle spasm  often throwing the victim
from the source  a shorter duration of exposure
but  the likelihood of traumatic blunt injury.
• Alternating current (AC):
– 3x > dangerous than DC (same voltage)
– continuous muscle contraction, or tetany 
occurs when the muscle fibers are stimulated at
40-110x/ second
http://ehs.okstate.edu/modules/electric/Emergency.htm
http://www.uic.edu/labs/lightninginjury/treatment.html
Electrical Burns - Acute Care

A - Airway
B - Breathing
C - Circulation
D - Disability
E - Expose The Patient
http://www.uic.edu/labs/lightninginjury/treatment.html
Chemical Burns
• Chemical injury can result from exposure to acids, alkalies,
and petroleum products.
• Alkali burns are generally more serious than acid burns,
because the alkalies penetrate more deeply.
Etiology
• Acids
– Sulfuric acid
– Nitric acid
– Hydrofluoric acid ( not cause immediate burning or
pain on contact)
– Chloroacetic acids
• Monochloroacetic acid (highly corrosive)
• Dichloroacetic acid
• Trichloroacetic acid
– Phenol and cresols (substances are very irritating to
the skin and can be absorbed through the skin to
produce systemic toxicity.)
• Bases
– Sodium hydroxide and potassium hydroxide
– Calcium oxide
– Sodium and calcium hypochlorite
– Ammonia (cause severe skin burns as well as
pulmonary injury if inhaled)
– Phosphates
– Lithium hydride (produce thermal and alkaline
burns.)
Sign and symptoms
• Clinical signs and symptoms vary depending on
the route of exposure and the particular
substances involved.
• History:
– Offending agent, concentration, physical form, pH
– Route of exposure
– Time of exposure
– Volume of exposure
– Possibility of coexisting injury
– The timing and extent of irrigation
• If the exposure was by ingestion, the immediate concern is to
protect the patient's airway. If there is evidence of airway
compromise (eg, oropharyngeal edema, stridor, use of accessory
muscles), consider establishing a definitive airway.
• In dermal exposures, consider the following:
– Size
– Depth
– Location
– Circumferential burns
• In ocular exposures, consider the following:
– Visual acuity
• In the presence of periorbital dermal lesions, consider the
following:
– Scleral and corneal lesions (eg, ulcerations, fluorescein uptake)
– Leakage of vitreous humor
• For ingestions, consider the following:
– Presence of oral burns or edema, drooling
– Dysphagia, stridor, wheezing, dyspnea, tachypnea
– Abdominal tenderness, guarding, crepitus, subcutaneous air (Hamman
crunch)
Laboratory
• Laboratory studies depend on the burn • For ingestions of caustics, consider the
type and extent of exposure. following:
• For severe burns, consider the following: – Hemoglobin/hematocrit
– Electrolytes – Pulse-oximetry or ABG if respiratory symptoms
– Creatinine • For oxalic acid burns, check calcium.
– BUN • For chromic acid burns, consider the
– Glucose following:
– Urinalysis – BUN
– CBC count – Creatinine
– Creatine phosphokinase • For monofluoroacetic acid burns,
– Coagulation profile consider the following:
• For localized burns, usually no laboratory – Electrolytes
tests are required. – ABG
• For hydrofluoric acid burns, consider the • For phenol burns, consider the
following: following:
– Calcium – Electrolytes
– Magnesium – CBC count
– Potassium – Urinalysis
– Creatinine
– Liver function tests
• For ingestions, consider the following:
– Chest radiography if any respiratory symptoms
– Abdominal radiography (flat and upright) if signs
of peritonitis are present
Diagnose
• Endotracheal intubation is required for severe
respiratory symptoms. Direct visualization is
recommended to assess the degree of injury.
• Bullae resulting from chemical burns should
be decompressed and debrided
Treatment
• Pre-hospital
– Prevent contaminated irrigation solution from running
onto unaffected skin.
– Remove contaminated clothe
– Special situation:
• If contamination with metallic lithium, sodium, potassium, or
magnesium has occurredcovered with mineral oil and the
metallic pieces should be removed with forceps and placed in
mineral oil. If forceps are not available, soak the area with mineral
oil and cover it with gauze soaked in mineral oil.
• If contamination with white phosphorus has occurred. Keep the
area moist at all times. The area can also be covered with
petroleum jelly.
• If eye exposures have not been irrigated, then this should be
started immediately. Immediate removal of caustic substances in
the eye is critical
ED
• Using litmus paper to measure the pH of the affected area or the
irrigating solution
• Complete removal and neutralization of concentrated acids and
alkalis may require several hours of irrigation. Tap water is adequate
for irrigation.
• Hydrofluoric acid burns
– Fluoride can be neutralized by either calcium or magnesium.
– For small superficial burns, topical calcium or magnesium gels can be
applied.
– Deeper burns usually require subcutaneous injections of calcium
gluconate.
– Hand burns can be difficult to manage; these burns can be treated
with subcutaneous injections of calcium, intra-arterial calcium
infusions, or intravenous infusions of magnesium.
– Keeping the hand warm and adequately treating pain will help to
increase local circulation and the body's natural supply of calcium and
magnesium
• Caustic ingestions
– Gastric emptying is contraindicated.
– Activated charcoal is not useful and may interfere with
subsequent endoscopy.
– Dilution with milk or water is contraindicated if any degree
of airway compromise is present.
– Milk may interfere with subsequent endoscopy.
– Water is benign.
– Some substances, such as drain cleaners containing
sulfuric acid or sodium hydroxide, generate heat when
diluted with water.
– Local areas of heat generation can be minimized by
diluting with a moderate quantity of fluid (250-500 mL).
Head Injuries
• Head injuries are among the most common
types of trauma encountered in emergency
departments (EDs).
• A review of cranial anatomy includes
• Scalp
• Skull
• Meninges
• Brain
• Ventricular system
• Intracranial compartments
Classification
Skull Fractures
• Skull fractures may occur in the cranial vault or skull
base. They may be linear or stellate, and open or
closed.
• Basilar skull fractures usually require CT scanning
with bone-window settings for identification.
• The clinical signs of a basilar skull fracture include :
• periorbital ecchymosis (raccoon eyes)
• retroauricular ecchymosis (Battle’s sign)
• CSF leakage from the nose (rhinorrhea) or ear (otorrhea)
• N. VII and N.VIII dysfunction (facial paralysis and hearing
loss)
Skull Fractures
• Open or compound skull fractures can provide
a direct communication between the scalp
laceration and the cerebral surface, because
the dura may be torn.
• A linear vault fracture in conscious patients
increases the likelihood of an intracranial
hematoma by about 400 times.
Intracranial Lesions
• Intracranial lesions may be classified as diffuse
or focal, although these two forms frequently
coexist.
Diffuse Brain Injuries Focal Brain Injuries

• Diffuse brain injuries range from • Epidural Hematomas


mild concussions to severe • These hematomas typically become biconvex
hypoxic ischemic injuries or lenticular in shape as they push the
• Severe diffuse injuries often adherent dura away from the inner table of the
result from a hypoxic, ischemic skull.
insult to the brain due to • They are most often located in the temporal
prolonged shock or apnea or temporoparietal region and often result
occurring immediately after the from a tear of the middle meningeal artery as
trauma. the result of a fracture.
• CT scan : may initially appear • A lucid interval between time of injury and
normal, or the brain may appear neurologic deterioration is the classic
diffusely swollen, with loss of presentation of an epidural hematoma
the normal gray-white distinction • Subdural Hematomas
• Another diffuse pattern, often • They often develop from the shearing of small
seen in high-velocity impact or surface or bridging blood vessels of the
deceleration injuries, may cerebral cortex.
produce multiple punctate • on a CT scan, subdural hematomas more often
hemorrhages throughout the appear to conform to the contours of the
cerebral hemispheres, which are brain.
often seen in the border • Contusions and Intracerebral Hematomas
between the gray matter and • The majority of contusions occur in the frontal
Primary Survey & Resuscitation Secondary Survey
• Airway and Breathing • Serial examinations (e.g., GCS score,
• Early endotracheal intubation should be lateralization, and pupillary reaction) should
performed in comatose patients. be performed to detect neurologic
• The patient should be ventilated with 100% deterioration as early as possible.
oxygen until blood gas measurements are • A wellknown early sign of temporal lobe
obtained, after which appropriate (uncal) herniation is dilation of the pupil and
adjustments to the fraction of inspired loss of the pupillary response to light
oxygen (FIO2) are made.
• Pulse oximetry is a useful adjunct, and
oxygen saturations of >98% are desirable.
• Ventilation parameters are set to maintain a
PCO2 of approximately 35 mm Hg.
• Hyperventilation (PCO2 <32 mm Hg) should
be used cautiously in patients with severe
brain injury and only when acute neurologic
deterioration has occurred.
• Circulation
• Hypotension usually is not due to the brain
injury itself, except in the terminal stages
when medullary failure supervenes or there is
a concomitant spinal cord injury.
• Euvolemia should be established as soon as
possible if the patient is hypotensive, using
blood products, whole blood, or isotonic
fluids, as needed.
Medical Therapies for Brain
Injury Surgical Management
• Intravenous fluid • Scalp wounds
• Hyperventilation • Depressed skull fractures
• Manitol • Intracranial mass lesion
• Hypertonic saline • Penetrating brain injuries
• Barbiturates
• Anticonvulsants
Brain Death
• The diagnosis of brain death implies that there is no possibility for
recovery of brain function. Most experts agree that the following
criteria should be satisfied for the diagnosis of brain death:
• Glasgow Coma Scale = 3
• Nonreactive pupils
• Absent brainstem reflexes (e.g., oculocephalic, corneal, and Doll’s eyes,
and no gag reflex)
• No spontaneous ventilatory effort on formal apnea testing
• Ancillary studies that may be used to confirm the diagnosis of brain
death include:
• Electroencephalography: No activity at high gain
• CBF studies: No CBF (e.g., isotope studies, Doppler studies, xenon CBF
studies)
• Cerebral angiography

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