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Acute lung injury (ALI) is associated with an insult to endothelial and epithelial cells in the lung resulting in release of mediators, increased vascular- and alveolar permeability, interstitial edema formation, alveolar collapse, and thereby arterial hypoxemia []–[]. Although acute respiratory distress syndrome (ARDS) was initially believed to be caused by a diffuse lung injury, computed tomography (CT) of patients with ARDS revealed radiographic densities corresponding to alveolar collapse localized primarily in the dependent lung regions, which correlate with intrapulmonary shunting and account entirely for the observed arterial hypoxemia. Thus, intrapulmonary gas is unhomogeneously distributed during ARDS due to uneven distribution of injury, regional surfactant dysfunction, pulmonary infiltrations and/or alveolar collapse. Positive pressure ventilation, commonly used to improve gas exchange, may further aggravate preexisting lung injury including pneumothorax, alveolar edema, and alveolar rupture [, ].

Capnography has become standard of care in monitoring respiratory function during anesthesia [] and together with pulse oximetry has contributed to a major improvement in safety and reduction in morbidity over the last three decades [].

Since Galen’s description 2000 years ago that the lungs could be inflated artificially, mechanical ventilation has become a primary intervention for life support []. The common indication for mechanical ventilation is respiratory failure, defined as a major abnormality in gas exchange []. According to Esteban et al. [], how the assist is delivered in terms of volume and respiratory rate varies widely among centers. Recent randomized clinical trials have suggested that limitation of tidal volume reduces the risk of ventilator-induced lung injury (VILI) [].

How does one predict which patient can be successfully extubated and removed from mechanical ventilation? This is usually simple in patients with known good pulmonary function prior to an acute, now reversed, event (e.g., drug overdose with central nervous system depression or surgery) in whom no new acute compromising event has occurred (e.g., aspiration, stroke). It is not simple in patients recovering from a prolonged ventilatory or respiratory illness that required mechanical ventilation or when a short acute ventilatory illness is superimposed on a chronic condition that may compromise respiratory reserve (Table 1). In this latter situation, knowledge and use of measures that allow some degree of prediction of readiness for withdrawal (liberation) from mechanical ventilation are often useful.

Endotracheal intubation and mechanical ventilation are required for the majority of critically ill patients suffering from acute brain injury. While these patients certainly may develop cardiopulmonary complications, many of them receive mechanical ventilation because of a decreased level of consciousness and subsequent inability to protect the airway and clear secretions, rather than because of primary respiratory failure. Indeed in a large observational study of mechanical ventilation practices around the world, coma was the primary reason for initiation of ventilatory support in close to 20% of cases []. In addition, many brain-injured patients will need ventilatory support as part of the management of raised intracranial pressure (ICP) []. For example, severe stroke patients may not have underlying respiratory insufficiency but up to 25% of them require mechanical ventilation []. Like all patients receiving invasive ventilation, patients with acute brain injury are at risk of complications including airway injury and ventilator-associated pneumonia (VAP); as usual our goal is to discontinue ventilatory support as soon as it is safe to do so. However, the approach to weaning and discontinuation of mechanical ventilation in this patient population remains a challenge to clinicians as these patients have been understudied and because the usual cardiopulmonary markers of liberation readiness may not be applicable. In this chapter, we will discuss what is currently known about weaning and discontinuation from mechanical ventilation, as well as tracheostomy, in brain-injured patients.

Mechanical ventilation is a life-support procedure widely used in patients with severe respiratory failure. Despite its benefits, this technique is associated with various complications that can be classified into three categories [, ]: When clinicians decide to proceed to withdraw mechanical ventilation, they have to assess different weaning parameters, trying to avoid unnecessary delays and to assure the success of this process . Although a large number of patients who have recovered from the episode of acute respiratory failure may be successfully extubated, 6 to 23% of them will need re-intubation within 48 to 72 hours after extubation [, ], with remarkable consequences on their clinical outcomes [, ]. We will review the impact and the etiology of respiratory failure after extubation, as well as the use of non-invasive ventilation (NIV) in the management and prevention of respiratory failure after extubation.

One of the detrimental complications of burns is the onset of acute lung injury (ALI). In patients with extensive cutaneous burns in which the burned area exceeds 30% of the total body surface area, capillary hyperpermeability occurs not only at the injured site but also in regions distant from the initial insult [, ]. The vascular hyperpermeability leads to a large amount of fluid flux from the circulating plasma to the interstitial spaces. This lung edema formation is even more severe when the thermal injury is associated with smoke inhalation eventually leading to acute respiratory distress syndrome (ARDS) []. Previously, we designed an ovine model of combined burn and smoke inhalation injury and described the patho-physiology of ALI []. The ALI in combined burn and smoke inhalation injury is characterized by severe deterioration of pulmonary gas exchange (decrease in PaO/FiO, and increase in pulmonary shunt fraction), pulmonary microvascular leakage with subsequent formation of interstitial edema which is evidenced by increased pulmonary transvascular fluid flux (increased lung lymph flow), increased lung water content (lung wet-to-dry weight ratio), and increased pulmonary vascular permeability to both fluid and protein. These pathological changes are associated with severe pulmonary hypertension, massive airway obstruction by obstructive cast material, and increased ventilatory (peak and pause airway) pressures. In previous studies, we have also evaluated factors that play a crucial role in patho-genesis of ALI. There are several pathogenic factors, which affect the pulmonary function.

The changes in patient metabolism following a major burn may be seen for more than 12 months after the initial injury. The ensuing period of hypermetabolism and catabolism post-burn leads to impaired immune function, decreased wound healing, erosion of lean body mass, and hinders rehabilitative efforts delaying reintegration into normal society. The typical changes in metabolism are the development of a hyperdynamic circulation [], increased body temperature [], increased protein catabolism with peripheral protein wasting [], increased lipolysis leading to fatty infiltration of the liver [], increased glycolysis and futile substrate cycling . These changes are responsible for much of the morbidity and mortality seen with such an injury and as such are important targets for available treatments including: early excision and grafting; aggressive treatment of sepsis, early commencement of high protein, high carbohydrate enteral feeding, elevation of the immediate environmental temperature to 31.5°C (±0.7°C); and early institution of an aerobic resistive exercise program. Several pharmacotherapeutic options are also available to further reduce erosion of lean body mass; these include anabolic agents such as recombinant human growth hormone, insulin, oxandrolone and beta-blockade with propranolol. This chapter will discuss the metabolic changes seen following a major burn and how different treatment options affect outcome.

Multiple organ failure (MOF) and compromised immune function, which results in increased susceptibility to sepsis, remain major causes of burn morbidity and mortality []. The major frustration for the burns team is for the patient to survive the critical care period, only to succumb to infection, which is known to cause over 75% of burn deaths [].

By elevating the blood cortisol level, the body attempts to adapt to stress associated with severe disease, trauma, surgery, and particularly sepsis [–]. Although primary insufficiency of the hypothalamus-pituitary-adrenal (HPA) axis is rare in the critically ill, relative adrenal insufficiency has been considered as a frequent complication of septic shock and other critical conditions [, , –]. In these conditions, the cortisol level, despite being normal or even elevated above normal, is considered inadequate for the degree of stress, as manifested by a subnormal rise of the cortisol level in response to additional stimuli [, , , , –]. The latter could indicate a transiently diminished adrenal reserve following adrenal exhaustion, in the absence of structural defects [, , ]. In contrast, primary adrenal insufficiency is caused by destruction or failure of the adrenal cortex. Conversely, various terms have been used in the critically ill, including adrenocortical deficiency, hypocortisolemia, functional or occult hypoadrenalism, adequate and inadequate cortisol production, and non- or hyporesponsiveness (to adrenocorticotropic hormone [ACTH]). We will lump these together as relative adrenal insufficiency (and non-responsiveness to ACTH), as opposed to primary or secondary adrenal insufficiency with failure of adrenal or hypothalamus/pituitary, respectively [, –].