Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4581_Библиотеки_им_академика_М_И_Перельмана

2017). NO may also interact with the superoxide

direct effects of a burn are due to disruption of the normal functioning of the skin. Among oth­ers, sensation, ability to prevent water loss, elec­trolyte balance, and ability to control body temperature are deranged and eventually lost. In larger burns (>30% of total body surface area, TBSA), there is a signicant inammatory response, which results in increased leakage of uid from the capillaries and subsequent tissue edema. There is signicant plasma loss and sub­sequent hemoconcentration. Poor blood ow to organs such as the kidneys and gastrointestinal tract may result in renal failure and gastric ulcers. Additionally, severe burns induce response that affects skeletal muscle, heart, lungs, liver, and nervous system (Nielson etal. 2017). Increased levels of catecholamines and cortisol, muscle wasting, and insulin resistance cause a hypermet­abolic state that can last for years. This is associ­ated with increased cardiac output and metabolism, tachycardia, and poor immune func­tion. Burn patients are prone to infections, and sepsis is one of the main reasons of fatal outcome in patients with extensive burns.

2007). Initially, carbon monoxide poisoning,

hypoxia, and thermal injury occur. Subsequently (24–72h), pulmonary edema, atelectasis, and tra­cheobronchitis develop. There is damage to the airway and alveolar epithelium, with sloughing of the mucosa (Fig. 11.3) and formation of mucous plugs and casts which can cause obstruc­tion and air trapping (Nugent and Herndon 2007). The third phase is bronchopneumonia, typically occurring 3–10 days after injury, which results due to impaired lung defense mechanisms such as the mucociliary system and alveolar macro­phages, and abnormal lung function and ventila­tion (Nugent and Herndon 2007). Respiratory failure and acute respiration distress syndrome can develop from the inhalation injury. Signs and symptoms that should evoke suspicion of an inhalation injury include dyspnea, hoarse voice, cough, anxiety or agitation, stridor, wheezing, facial burns, singed nasal hairs, production of carbonaceous sputum, or presence of carbona­ceous material in the oral cavity (Sheridan 2000). One of the most useful tools for the assessment of inhalation injury is the ber-optic bronchoscope (Sheridan 2000). This allows assessment of the airway mucosa and patency of the supraglottic airway, thus identifying patients at risk for air­way occlusion. Carbonaceous material in the

supraglottic and the tracheobronchial tree, edema, hyperemia, and mucosal sloughing/ breakdown of the tracheal mucosa can also be seen (Fig. 11.3). Bronchial toilet and specimen collection are facilitated. In the study of Ching etal. (2016), bronchoscopy proved useful in pre­dicting mortality, days of ventilation, and dura­tion of intensive care unit (ICU) admission. Bronchoscopy can be performed under local anesthesia. Less commonly utilized is xenon-133 ventilation-perfusion scanning. Areas demon­strating delayed excretion of the xenon isotope by the lung delayed indicate regions of small air­way partial or total obstruction (Moylan Jr etal.

rst, second, or third degree, depending on the depth of a burn, has been replaced by the des­ignations of epidermal, supercial dermal, deep dermal, and full thickness. Burns involv­ing only the epidermis are erythematous and painful but do not form blisters (Fig. 11.4).

Within 3–4days, the dead epidermis sloughs and is replaced by regenerating keratinocytes. Supercial dermal burns (Fig. 11.5) extend into the papillary dermis and characteristically form blisters. With appropriate care, super­cial dermal burns usually heal within 2–3weeks without the risk of scarring and therefore do not require an operation. Deep dermal burns extend into the reticular dermis and generally will take 3 or more weeks to heal. They also blister, but the wound surface appears mottled pink and white immediately following the injury (Fig.11.6). Discomfort and pressure are the patient’s main complaints, rather than pain. When pressure is applied to the burned area, capillary rell shows slowly or is absent. The wound is often less sensitive to pinprick com­pared to the surrounding normal skin. By the second day, the wound may be white (Fig.11.2) and is usually fairly dry. Partial-thickness burns that are predicted not to heal by 3weeks should be excised and grafted. Full-thickness burns involve the entire dermis and extend into subcutaneous tissues. Their appearance may be charred (Fig. 11.7), leathery, rm, and depressed when compared to adjacent normal skin. These wounds are insensitive to pinprick and light touch. They may be mottled in appearance; they do not blanch on pressure and may have a dry, white appearance. Full­thickness burns should be excised and grafted early to expedite the patient’s recovery process and prevent infection and hypertrophic scar­ring. Differentiating a deep dermal from a full­thickness burn can be quite difcult initially. Revisions of burn depth estimations are often necessary in the rst 24–72h. As evidenced by histologic studies, a burn injury is a dynamic process that peaks at about 3 days (Boykin et al. 1980). Initial evaluation by an experi­enced surgeon as to whether such an “indeter­minate” dermal burn will heal in 3 weeks is only about 50–70% accurate (Hlava etal. 1983; Yeong et al. 1996). A number of techniques have been developed to improve clinical judge­ment. Laser Doppler is one of the most recent and widely studied of these techniques. It pro­vides an estimate of perfusion through the burn

wound, the assumption being that a lower per­fusion correlates with a deeper wound and, therefore, a longer time to heal (Yeong et al.

1996; Jaskille etal. 2010). The accuracy in the

The location of a burn may have serious

wound by stabilizing skin mast cells and decreasing histamine release. Because of the lim­ited surface area burned among most of the patients with only face/neck burns, the detrimen­tal side effects of active cooling, e.g., hypother­mia, should not occur. Removal of residual dirt and cleansing of the wound can be accomplished with room temperature or tepid normal saline or water with a mild, bland soap. Antiseptic solu­tions (chlorhexidine gluconate solution, povi­done-iodine solution) should be used with caution because according to some reports these agents can inhibit the healing process. An appraisal of povidone- iodine and wound healing, however, concluded that these preparations do not have deleterious effect on wound healing (Goldenheim

1993). The effects and safety of antiseptics were

recently assessed by Norman etal. (2017). The authors concluded that it is uncertain whether antiseptics are associated with any difference in healing, infections, or other outcomes. Where there is moderate or high certainty evidence, decision makers need to consider the applicabil­ity of the evidence from the comparison to their patients (Norman et al. 2017). Tar and asphalt residues can be removed by solvents that have a close structural afnity to these substances (e.g., substances related to petrolatum). Medi-Sol™ Adhesive Remover (a citrus-based, nontoxic, nonirritating Category 1 Medical Device solvent authorized by the FDA for use in the skin) has been reported to be an effective product for the removal of tar and asphalt (Stratta etal. 1983).

Topical antibiotics have been recently sug­gested for the removal of adherent asphalt. The use of topical agents is discouraged, because they are likely to result in tissue toxicity (Bosse etal.