Debridement and wound care is commenced in the burn unit. This is typically done in a heated hydrotherapy room with use of warm water to minimize heat loss. At this time, any loose skin and blisters are debrided and topical agents are applied.
Effective debridement of burn eschar increases penetration of topical agents, improves time-to-healing for partial-thickness burns, and may allow faster skin graft coverage of full-thickness burns. Administration of appropriate analgesia, oral or intravenous, is very important throughout the debridement process. A number of topical antibiotics are for sale to application to lose wounds.
A combination of xeroform and bacitracin is often used for superficial partial- thickness burns. This application has got the benefit of being relatively inexpensive and widely available and it is put on every day basis until reepithelialization has occurred.
Silver sulfadiazine is easily the most widely used topical agent for deep partial-thickness burns or partial-thickness burns of indeterminate depth as well as full-thickness burns. It can be applied either daily or twice daily. In vitro studies have shown silver sulfadiazine to become active against gram-positive and gram-negative bacteria, and Candida albicans.
Minimal pain is assigned to its application and in fact, many patients think it is soothing when applied to partial-thickness burns. The development of a pseudoeschar is one detriment of silver sulfadiazine and may render resolution of burn depth difficult. Other downsides of its use include leukopenia and also the chance of induction of resistant organisms such as Pseudomonas aeruginosa or Enterobacteriaceae.
Silver nitrate has significant antimicrobial properties and it is nontoxic in its most commonly used formulation. It is important to keep in mind, however, that gram-negative bacteria and some gram-positive bacteria may reduce silver nitrate to silver nitrite be responsible for methemoglobinemia in rare cases. It's active against gram positive and some gram negative bacteria, for example Pseudomonas aeruginosa, and is now commonly incorporated into commercially accessible wound maintenance systems.
Mafenide includes a broad antibacterial spectrum and it has the very best eschar penetration of any available agent. Because of its efficient penetration of cartilage, it is used over cartilaginous areas like the nose or the ear. It is almost always applied two times a day and due to its action as a carbonic anhydrase inhibitor could cause a metabolic acidosis if put on large surface areas. Of the silver containing products, Sulfamylon is the most painful to the patient.
Currently, inhalation injury is a more common acute reason for death from a burn injury compared to surface burns themselves. The mechanisms of injury may involve deadly carbon monoxide inhalation, thermal injury to top of the airway and digestive tract, and inhalation of the products of combustion.
Carbon monoxide (CO) is really a tasteless, odorless gas. It preferentially binds to hemoglobin and displaces oxygen from the hemoglobin molecule thereby impairing tissue oxygenation. The major deleterious results of carbon monoxide result from its displacement of oxygen. It is estimated that it has more than 200 times the affinity for hemoglobin than oxygen.
The most typical reason for direct thermal problems for the upper airway is inhalation of steam. The reason being steam has 4000 times the heat-carrying capacity of air. Edema from the face and perioral tissues can result in narrowing of the airway and increased work of breathing. In addition to direct thermal injury to the airway, edema from the airway often parallels the generalized edema in a burn patient. Therefore, airway protection should always be kept in mind in a patient with severe generalized burn edema.
Inhalation of aldehydes, ketones and organic acids, all products of combustion, is easily the most significant element of inhalation injury. The suggestions above chemicals cause significant chemical injury to the respiratory system and mimic aspiration of acidic gastric contents.
Increased capillary permeability and alveolar injury can lead to pulmonary edema and ultimately adult respiratory distress syndrome (ARDS). Secondary pneumonias may develop after plugging of the lower airways with sloughed bronchial mucosa. Patients with secondary pneumonias after inhalation injury possess a poor prognosis.
A history of a flame burn in an enclosed space, singed nasal hairs and facial or oropharyngeal burns, and also the presence of carbonaceous sputum should raise suspicion of the inhalation injury. CHgb levels should be obtained in all patients with such findings. Levels above 10% are significant and denote inhalation injury and levels above 50% are associated with a high likelihood of death.
A patient with documented inhalation injury should be immediately positioned on 100% oxygen therapy which cuts down on the washout time of carbon monoxide. Fiberoptic bronchoscopy from the upper respiratory tract is the defacto standard for diagnosis and could show edema from the vocal cords and charring, sloughing, or edema from the hypopharyngeal and upper tracheal mucosa.
The management of inhalation injury is primarily supportive care. Endotracheal intubation should be performed liberally because of the potentially disastrous consequences of the delay in diagnosis. If deadly carbon monoxide poisoning is present, 100% oxygen is administered. Furthermore, the airway can be cleared of mucosal plugs and airway debris by aggressive pulmonary toilet and bronchoscopy.
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