**Table 3.**

*Clinical Management of Shock - The Science and Art of Physiological Restoration*

stress disorder [170–173].

hyperdynamic phase begins, cardiac output may exceed 1.5 times that of a normal baseline. Increases in cardiac output entail much greater cardiac work and overall energy expenditure. For these reasons, propranolol is highly efficacious during acute care in burn patients [169]. In fact, long-term propranolol administration initiated in the acute setting decreases cardiac work, decreases lipolysis, improves nitrogen balance, helps restore insulin sensitivity, and mitigates post-traumatic

**9. The importance of endocrine system, including glycemic control**

ventilator, and hospital length of stay [177, 178, 182].

**10. Comment on inhalation injury**

As part of the hypermetabolic response to burn injury, significant increases in catecholamines, glucagon, and cortisol stimulate rapid glycolysis-gluconeogenesis cycle gyrations [174]. The result is the appearance of hyperglycemia and a concurrent state of insulin resistance. The magnitude of the overall effect appears to be dependent on the severity and size of the burn injury [175]. The administration of insulin to maintain a serum glucose goal of ≤120 mg/dL has proven to be effective in attenuating some of the hypermetabolic changes that take place immediately after injury [176]. Insulin administration has been shown to improve muscle protein synthesis, normalize mitochondrial function, reduce oxidative stress, limit lean muscle mass loss, accelerate healing time, and improve long-term rehabilitation [176–179]. In addition to the normalization of serum glucose levels, the reduction in glycemic variability may be equally important [180, 181]. Other beneficial effects of goal-directed insulin therapy have been identified, including potential reductions in mortality, infections, sepsis, acute kidney injury, multiple organ failure, days on a

Although beyond the scope of the current chapter, various other endocrine system components are affected—both acutely and chronically—following burn injury [178, 183–188]. This includes the thyroid hormone metabolism [183, 184], the hypothalamic–pituitary axis [185], the renin-angiotensin system [185, 187], the reproductive system [185], among others [186]. Additional important endocrine considerations include the effects of exogenous hormone therapies, such as oxandrolone, recombinant human growth hormone, and incretin analogs [188]. Readers

Inhalation injury requiring mechanical ventilation is associated with increased mortality and greater volume of fluid resuscitation [189–191]. Carbonaceous debris in or around the mouth, facial burns, and singed facial or nasal hair are often cited as important clues during the BPE with respect to the presence of inhalation injury [192, 193]. However, the history of closed space smoke exposure is perhaps the most important clue as to whether or not a patient might have sustained an inhalation injury. Unlike burn injuries to the skin and subdermal tissues, which are primarily thermal in nature, inhalation injury is primarily a result of chemical exposure of tracheo-bronchial and pulmonary tissues to toxic products of combustion [191, 194, 195]. Primary thermal injury to the airway is often limited to the supraglottic region [195]. Diagnosis of lung injury is graded on a standardized scale from 0 to 4 based on bronchoscopic findings of airway edema, inflammation, mucosal necrosis, tissue sloughing, and presence of soot and carbonaceous material in the airway (see

are referred to the primary sources listed above for further information.

**154**

**Table 3**) [195].

*Description of inhalation injury severity grading based on bronchoscopic evaluation.*

If there is any concern for inhalation injury based on the initial or subsequent BPE, patient should be placed on 100% oxygen via non-rebreather mask and undergo measurements of blood carboxyhemoglobin and cyanide levels [196, 197]. In patients with early evidence of upper airway edema or impending respiratory failure as suggested by oxygen saturations below 92% and the simultaneous presence of tachypnea with hypercapnia, intubation should be expeditious [128, 198, 199]. Ventilator management for these patients is similar to ARDS using low tidal volumes and pressure control ventilation with permissive hypercapnia (as high as PaCO2 of 60 mmHg) [200, 201]. Additionally, sloughing of the injured pulmonary lining requires aggressive pulmonary toilet, chest physiotherapy, frequent suctioning, bronchoscopic removal of casts, and nebulizer therapy [128, 202, 203]. Various nebulizer combinations and frequencies of albuterol, heparin, acetylcysteine, hypertonic saline, and racemic epinephrine should be considered on a case by case basis depending on injury severity and clinical progression [128]. Patients should be closely monitored for development of ventilator-assisted pneumonia considering their primary injury has induced a transient immunosuppressed state—a factor that is further exacerbated by the presence of inhalation injury [204, 205]. Finally, for patients with very severe inhalation injury who continue to worsen despite maximal traditional mechanical ventilatory support, the use of high-frequency oscillatory ventilation may be indicated [206, 207].
