Current disease stratification tools of acute and chronic liver failure are inadequate, and therefore, it is difficult to effectively predict which patients are at risk or how risk evolves over time. Understanding the pathobiology, and the development of risk stratification using molecular and computational techniques would potentially guide risk stratification, permit trials targeted to mitigate injury, improve organ allocation and decrease mortality.
A better understanding of serum inflammatory mediators and biomarker patterns in acute liver failure might help distinguish spontaneous survivors from non-survivors and allow for the use of immunomodulatory therapy to improve outcomes and potentially decrease the use of liver transplants.
There appears to be a need for the validation in children of criteria used in adults to diagnose acute pancreatitis including prospective studies that standardize etiological classifications.
The natural history of pancreatitis in children needs to be better established in order to understand factors predicting disease severity, complications and the progression to MODS.
A better understanding of the molecular details associated with acute pancreatitis and their relationship to MODS needs to be attained.
The mechanisms by which acute kidney injury precipitate dysfunction in other organs are not clearly established; conversely, the mechanisms by which the kidney is secondarily injured as part of MODS are also not well understood.
An expansion of the understanding of the manner by which the hyperdynamic metabolic and catabolic responses associated with major pediatric burn contribute to the risk of MODS may result in better outcomes.
Further work assessing the genomic and proteomic profiles associated with burn injury may help to improve morbidity and mortality and reduce the incidence of MODS in this patient population.
A better understanding of the inflammatory and counter-inflammatory changes associated with major trauma is needed; such insight might afford opportunities to intervene and mitigate the occurrence and severity of associated MODS.
The natural history of trauma associated coagulopathy in children needs to be better delineated and understood in the context of injury severity. The role of thromboelastography driven resuscitation protocols in decreasing the morbidity and mortality associated with pediatric trauma warrants investigation.
A decision-making structure is needed to guide red blood cell transfusion both in terms of timing and amount based upon outcome-linked physiologic O2 delivery targets.
The ability to quantify O2 delivery and consumption measurements, to relate these measurements to O2 sufficiency and reserve at the whole body, organ, and tissue levels, and to attribute these parameters to anemia must be developed.
