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Volume 4
Clinical Pediatric Dermatology
ISSN: 2472-0143
Page 61
JOINT EVENT
Wound Congress 2018 &
Clinical Dermatology Congress 20
18
October 15-16, 2018
October 15-16, 2018 Rome, Italy
&
5
th
International Conference on
Advances in Skin, Wound Care and Tissue Science
14
th
International Conference on
Clinical Dermatology
Inhalation burn, crush-syndrome and rhabdomyolysis syndrom
Dalamagka Maria
1
and
Zervas Konstantinos
1
1
General Hospital of Larissa, Greece
I
nhalation burn is responsible for 50% of the mortality associated with thermal burn. Inhalation burns are usually observed
in exposure to smoke, heat, toxic gases, and combustion components. Inhalation burn causes damage to airway epithelium,
mucosal edema, and reduces surface activity. These conditions are clinically manifested by airway obstruction, bronchospasm
and atelectasis. The area above the tongue is particularly vulnerable to thermal damage. Often the burn develops swelling and
obstruction of the upper airways which may not be immediately apparent. The larynx can be affected not only by thermal burn
but also by the direct toxic action of irritant gases, showing early tibial swelling and laryngospasm. Unlike the upper airway
lesions, lesions of the tracheobronchial tree are almost never caused by heat. Heat burn of the lower airways is only observed
in exceptional cases of fire in a saturated water vapor environment. The lesions are usually of a chemical nature of irritating
gases and soot. The diagnosis is usually based on clinical behaviors such as: facial burns, soot deposition in the rat, pharynx,
epiglottis and tongue, voice gurgle, laryngospasm image and bronchospasm. Smoke exfoliation is also a positive diagnostic
point. Determining the level of carboxyhemoglobin is useful, but it is not always feasible. Chest X-ray (initially may not have
abnormal findings) and bronchoconstriction help estimate the extent of the lesion. In carbon monoxide poisoning (CO),
monoxide antagonizes oxygen is linked to hemoglobin, moves release curve of oxyhemoglobin to the left and thus leads to
tissue hypoxemia. The affinity of carbon monoxide for hemoglobin is 250 times greater than oxygen and the relatively low
concentration of inhaled monoxide causes high levels of carboxyhemoglobin. Two principles are the basis for the successful
treatment of CO poisoning: (a) maximizing the supply of oxygen to the tissues; and (b) using high oxygen concentrations in
order to accelerate the elimination of CO. If the patient inhales air, the half-life (T½) of carboxyhemoglobin is 2 to 3 hours. Upon
inhalation of 100% O2 this time is reduced to 20-30 minutes. Hyperbaric oxygen therapy is a healing method in severe cases.
The burning of natural material (wood, wool, silk) and certain synthetic substances such as nylon and polyurethane causes
the release of cyanide with the most important hydrogen cyanide. Their poisonous action is due to the binding of cytochrome
oxidase and inhibition of oxygen uptake at the cellular level. Cyanide poisoning should be suspected of any victim of fire in
an enclosed space where unexplained metabolic (lactic) acidosis occurs. Concentration of lactate> 10 mmol / L indicates a
high probability of cyanide poisoning. Blood cyanide concentration greater than 40 mmol / L is considered to be toxic, with
a concentration of 100 mmol / L being fatal. The clinical picture includes tachypnea, tachycardia, confusion, convulsions,
metabolic acidosis, and at higher concentrations of respiratory depression and circulatory insufficiency. The specific treatment
of cyanide intoxication involves the administration of 25% sodium thiosulphate at a dose of 50 ml at an infusion rate of 2.5
ml / min, which converts cyanide into thiocyanates that are less toxic and are eliminated by the kidneys. Also reported is
the administration of hydroxybutylamine (Vit B12) which binds cyanide to the formation of hydroxycyanocobalamin. The
dose used is 5 g at slow intravenous infusion. Burn injury is characterized by the development of burnout. Burning shock
is due to a combination of hypovolemia and local and systemic secretion of a large number of mediators of inflammation.
The most popular equation for calculating liquids is the Parkland equation: R / L 4ml × body weight (kg) ×% EU; 50% of
the volume of fluid is given in the first 8 hours, the rest - 16 hours; If the EU assessment is not feasible, it is recommended to
administer 20 ml / kg of body weight ; crystalline solutions during the first hour of injury • the first 24 term is recommended
to use only crystallized solutions. Factors which increase the needs of the liquids delivered: Inhalation burns; Delay in fluid
delivery; Electric burn; Extensive extent of burn surface; Concurrent injuries; In recent years, the so-called "fluid creep"
phenomenon has been described Crush-syndrome and rhabdomyolysis syndrome: It was first described after a London
bombing during the Second World War. The syndrome occurs during natural disasters, wars, explosions, industrial accidents.
Compression of muscle mass leads to tissue ischemia, an increase in tissue pressure, which exceeds the capillary filtration
pressure. After lifting the external pressure, the muscle tissue is reperfused. The mechanism of ischemia-reperfusion injury is
the major pathophysiology-logical mechanism of this syndrome. Often, pressure damage is associated with vascular damage,
traumatic vascular rupture, thrombosis and stroke. Occlusion syndrome is clinically manifested by hypoemia sequelae due to
high accumulation of fluids in damaged tissues and by seo resulting from the release of large amounts of toxic substances from
Clin Pediatr Dermatol 2018, Volume 4
DOI: 10.21767/2472-0143-C2-006