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In critically ill patients, artificial nutritional support is now considered to be the standard of care, as it improves wound healing [], reduces complication rates [], and improves clinical outcomes [], []. A multicenter, cluster-randomized clinical trial investigating the dissemination and practice of evidence-based algorithms for nutritional support in intensive care unit (ICU) patients demonstrated that the use of evidence-based algorithms (as opposed to standard clinician-driven management of nutritional support) increased the amount of nutritional support delivered (8.5 versus 6.9 days per 10 patient days; p = 0.02) and this led to reduced hospital length of stay (25 versus 35 days; p = 0.003) and a trend toward reduced mortality (27 v. 37%; p= 0.058) [].

Following injury, stress, infection or surgery, most critically ill patients have evidence of an increased metabolic response and protein catabolism, a result of the release of cytokines and other inflammatory mediators [,]. Early enteral feeding has been the recommended method of artificial feeding in these patients but is frequently associated with inadequate delivery of calories and nutrients []. In addition, feeding generally receives a lower priority when compared to hemodynamic resuscitation, modes of ventilation or control of septic shock. In this chapter, the deleterious effects of underfeeding will be emphasized, new tools for tight energy control will be proposed and specific conditions like severe obesity will be discussed.

The term and concept of atypical pneumonia appeared in the 1940s following observations of penicillin-resistant pneumonia []. Despite the identification of a large number of microorganisms, the challenge of isolating so-called ‘atypical’ bacteria is the principal cause of failure of the etiologic diagnosis of pneumonia. These pathogenic agents in the tracheobronchial tree include a large variety of bacteria, viruses and even protozoa. Among atypical bacteria, , and are the most widespread. Numerous other bacteria are emerging pathogenic species whose virulence is currently being evaluated. Clinical examination only provides a diagnostic orientation in a restricted number of cases. The availability of rapid and specific microbiologic examination improves the diagnostic performance for this type of pneumonia (Table 1) []. Since most of these bacteria are intracellular, diagnosis is based principally on serology.

Antibiotic resistance is an increasingly common problem in the contemporary health care system, and in particular, in the intensive care unit (ICU) [, ]. Critically ill patients are five to ten times more likely to develop a hospital-acquired infection than patients on a general hospital ward, and antibiotic-resistant pathogens are responsible for more than half of these infections [, ]. A better understanding of the factors responsible for the emergence of resistant pathogens in hospitalized patients is fundamental to the control, or reversal of this trend.

Invasive fungal infections are a growing problem in the intensive care unit (ICU), with species being the most common cause of these infections. is now the forth or fifth most frequent pathogen isolated from bloodstream infections [],[]. In 2004, in order to summarize current knowledge about treatment of the different forms of invasive candidiasis, new guidelines for the treatment of candidiasis were published by experts on behalf of the Infectious Diseases Society of America (IDSA) []. The application of these guidelines to the treatment of systemic candidiasis in the ICU will be discussed, as well as new combination approaches to therapy, involving use of more than one antifungal agent.

Invasive candidiasis, which includes candidemia and severe infections, remains a dreadful complication in hospitalized patients with a prognosis comparable to septic shock []–[]. With incidences around 5 to 10 per 1000 intensive care unit (ICU) admissions, invasive candidiasis represents 5 to 10% of all nosocomial infections []. Difficult to diagnose, except for candidemia, which manifests only late in the course of the disease, early pre-emptive or empirical antifungal treatment has been shown to improve prognosis .

The incidence of fungal infections has increased dramatically over a 20-year-period by 207% []. Fungi are the fourth leading pathogen in nosocomial infections in the USA. Five percent of all cases of sepsis are caused by fungal infections. The incidence of candidemia, which constitutes the majority of fungal nosocomial pathogens, in non-neutropenic surgical patients is 9.8/10,000 intensive care unit (ICU) days []. The mortality associated with systemic fungal infections remains high (20–60%). New therapeutic options, like modern triazole derivates (e.g., voriconazole) and the new echinocandin agents (e.g., caspofungin) or lipid-formulations of amphotericin B provide new options for the antifungal treatment of surgical ICU patients. In the light of limited diagnostic options, considerable costs, and the high mortality of fungal infections, therapeutic strategies should be clearly defined in appropriate guidelines.

A central task in critical care medicine is the continuous maintenance of adequate tissue oxygenation. However, impairment of tissue perfusion and, thus, oxygenation is a common issue in critical care medicine, e.g., caused by anemia, cardiac failure or sepsis. If systemic oxygen delivery is reduced or maldistributed, certain organs may be impaired in oxygenation even before systemic markers of tissue dysoxia occur. Herein, the splanchnic region is particularly vulnerable in critical illness. Impaired splanchnic tissue perfusion and oxygenation play a crucial role in the development and maintenance of critical illnesses, e.g., the gastrointestinal tract may become the motor of sepsis and the multiple organ dysfunction syndrome. Thereby, the splanchnic region plays a role both as a target (e.g., through ischemia/reperfusion phenomena), but also as a source of the disease process (e.g., translocation of gastrointestinal endoluminal bacteria and toxins). Regarding the latter, continuous adequate microcirculatory oxygenation appears important to maintain the integrity of the gastrointestinal barrier function. The splanchnic region is not only affected by the disease process, but also by numerous therapeutic interventions, e.g., ventilation or drugs.

Liver failure is formally defined by the triad jaundice, coagulopathy, and encephalopathy. It can develop on a background of chronic liver disease as a result of acute decompensation (‘acute-on-chronic’ liver failure) as well as in the absence of pre-existing liver disease (acute liver failure ). Due to the central role of the liver in metabolism, acute liver failure, regardless of the underlying cause, often culminates in multiple organ dysfunction and is still associated with an extremely high mortality []. These extrahepatic complications, including hepatic encephalopathy, hepatorenal syndrome (HRS), and susceptibility to infections are major causes of death in patients with liver failure. Thus, prevention and therapy of extra-hepatic complications may help to improve outcome, as the liver itself bears the potential to regenerate. In this light, extracorporeal liver support to retard progression of multiple organ failure (MOF) seems an attractive option. Monitoring of liver function is then crucial to predict recovery and ultimate outcome and to identify those patients requiring liver transplantation.

Although acute liver failure and acute on chronic liver failure are distinct clinical conditions, they commonly result in progressive and refractory organ dysfunction and death. Activation of the systemic inflammatory response is central to the pathogenesis of vasodilatory shock and multiple organ failure (MOF) encountered in both these conditions. Acute liver failure is characterized as a syndrome of circulatory failure that in many ways is similar to septic shock. It is inherently difficult to discern the relative contribution of hepatocellular necrosis and sepsis to the systemic inflammatory reaction encountered in these patients. Irrespective of the inciting event, the end product is that of MOF and death. Therefore, it is important to elucidate the components of the inflammatory cascade ‘downstream’ to the inciting event.