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In critically ill patients the delivery of nutritional support (largely in the form of enteral nutrition) using evidence-based algorithms is associated with improved outcomes. Delivery of enteral nutrition into the stomach is relatively straightforward, however the high incidence of upper GIT intolerance due largely to poor gastric motility may result in inferior outcomes due to inadequate delivery of enteral nutrition and increased risk of VAP.

The delivery of enteral nutrition directly into the small bowel is a logical alternative as a means of reducing these complications. Although not conclusive, current evidence suggests that small bowel feeding is at least equivalent and may be superior to gastric feeding in terms of nutritional delivery and VaP rates. Unfortunately the clinical practice of small bowel feeding has been hampered by the logistic, technical, and time difficulties associated with placement of nasojejunal tubes.

The question of where best to deliver enteral nutrition in critically ill patients to provide optimal nutritional support and reduce feeding related complications remains unresolved. There may also be subgroups of the critically ill population who truly benefit from the early placement of a nasojejunal tube and further clinical research comparing gastric and small bowel delivery is awaited. Because of the logistical difficulties associated with nasojejunal tube placement, the development of newer tubes which have the potential to overcome these problems, such as the frictional nasojejunal tube, may offer this possibility.

Targeting energy delivery according to resting energy expenditure and achieving this goal using protocols, aggressive, early enteral feeding through duodenal tubes, or supplementary parenteral nutrition appears most likely to reduce the negative energy balance observed in most ICU patients, especially in the first days after admission. The resultant energy control may decrease the number of complications and improve morbidity. In obese patients, lower energy goals can be provided with similar results.

The diagnosis of pulmonary infection caused by and , and different species of , is often long and challenging although they are the major etiologic agents of pneumonia. For this reason, the treatment of these infections remains probabilistic. Advances in new diagnostic techniques, such as PCR sequencing, show the relative predominance of atypical organisms and serves to identify emerging pathogenic agents. Moreover, these techniques should clarify the correlation between common and atypical pathogens.

Escalating rates of antimicrobial resistance among Gram-positive and Gram-negative bacteria provide particular challenges for the treatment of critically ill patients.

Widespread empiric antibiotic therapy in the ICU has fostered the emergence and dissemination of resistant bacteria. However, strategies aimed at controlling antibiotic use have been only partially successful. Normal host-microbial interactions are complex, and inappropriate use of antimicrobials can disrupt this fine balance, with deleterious consequences for both host and micro-organism: the line between benefit and harm is a fine one. More rational administration of antimicrobial agents and more reliable and rapid diagnostic technologies, are key priorities for future development.

The incidence of systemic infection in the intensive care setting has been increasing over the last two decades. While continues to be the commonest species, and has the highest associated mortality, there has been an increase in other species of , such as and , which are more likely to be intrinsically resistant to fluconazole. Therefore, while current IDSA guidelines recommend amphotericin B deoxycholate, caspofungin or fluconazole as primary therapy for adult non-neutropenic patients with candidemia, it is prudent to avoid using fluconazole unless the isolate is known to be sensitive to this drug. Antifungal trials comparing these drugs have focused on patients with candidemia and as a result there is a lack of data on their comparative efficacy in other forms of invasive candidiasis, such as intra-abdominal candidiasis, which can be particularly difficult to treat. There appears to be little to choose between these drugs in terms of efficacy. Caspofungin and fluconazole are less toxic than amphotericin deoxycholate, but the toxicity of amphotericin B is much reduced if a lipid-associated formulation is used.

Combination therapy may provide a much needed means of reducing the morbidity and mortality of invasive candidiasis and reducing the emergence and spread of drug-resistant strains of , which are much more likely to occur on prolonged courses of suboptimal monotherapy. A potential combination is amphotericin B with the antifungal antibody Mycograb. The added cost of such drug combinations will need to be evaluated in the context of the cost of the disease itself, as well as the savings which result from reduced reliance on widespread antifungal prophylaxis and empiric treatment as more effective therapy for proven cases becomes available, and shortened courses of antifungal treatment are possible due to faster resolution of the infection.

Hemorrhage in blunt trauma usually derives from many contemporary bleeding sites, which may be stopped with surgery or interventional radiology. Protocol-driven management of specific injuries is mandatory to achieve the best results when a multi-disciplinary team is at work. However, a significant amount of blood loss may derive from small interrupted vessels, not amenable to surgical or angiographic control, especially in the case of traumatic coagulopathy. A pharmacological approach may be indicated to stop this so-called non-mechanical bleeding. Based on available data and on our experience, rFVIIa is a safe and useful adjunctive treatment to standard therapies in the management of critical hemorrhage in a selected trauma population. The drug is extremely expensive, but if it works and if we consider potential reduction of ICU days and, ultimately, life preservation, it may become a cost-effective treatment. However, large, prospective randomized, phase 3 trials are needed to answer some unresolved questions including optimal timing of administration, dosing and number of doses.

Although invasive candidiasis is a widespread problem, prophylaxis is not yet established. Large, multicenter, randomized clinical trials are lacking. Furthermore, the epidemiologic shift to non-albicans species, with their relevant fluconazole resistance, moves other agents into the field of interest for further studies. Otherwise, empirical and/or preemptive therapy, triggered by validated risk assessment procedures may be more valuable as prophylaxis. Emerging fungal infections in surgical ICU patients — caused by yeasts or molds — force us to establish new elaborate therapeutic strategies. We will see whether the outcome of our patients can be improved by implementation of these treatment protocols.

Since splanchnic impairment of perfusion and oxygenation triggers and perpetuates critical illness, including sepsis and MOF, it is crucial to elucidate the splanchnic effects of common clinical interventions applied in intensive care medicine. Herein, findings of experimental studies may serve to reduce the complexity of splanchnic pathophysiology and generate promising concepts to be tested in the clinical setting. Maybe we have to become familiar with the thought that there is not a single variable guiding our therapy of splanchnic hypoperfusion. Just as we have learned not to judge systemic hemodynamics by a single variable, future splanchnic monitoring tools will enable us to extend our ability to recognize patterns indicative of splanchnic hypoperfusion. Despite major advances in splanchnic monitoring techniques, a combination of easy-to-use and minimally-invasive metabolic and perfusion measurements allowing us to recognize pathophysiologic patterns in splanchnic perfusion and metabolism is not in sight. Ultimately, this concept should enable us to base our therapy on systemic splanchnic circulatory variables to improve outcomes for the critically ill.

Numerous international governments and federal funding agencies have placed the elimination of healthcare disparities on a spate of agendas targeted for completion in the next 10 to 20 years. Disparities in ICU patients are often less recognized, as efforts to identify and eliminate disparities frequently focus on common clinical conditions. Greater efforts are required to characterize the magnitude of healthcare disparities in critically ill patients and to seek the root causes of these disparities. The elimination of healthcare disparities will require different interventions depending on the type of disparities, the underlying cause(s) and the type of healthcare system in which they occur.

Monocyte dysfunction in the systemic inflammatory response plays a major role in the pathogenesis of organ dysfunction in acute liver failure and acute on chronic liver failure. Our understanding of the processes that lead to immune ‘dysregulation’ in these conditions is limited at present; however, patterns revealed in the studies reviewed above have offered insights into this hugely complex field. Hopefully, further studies into monocyte function will allow clinicians to recognize at risk patients, and perhaps develop new therapeutic strategies.