To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Multiple organ failure (MOF) can affect any organ and systems not thought of as organs such as endocrine, immune, haematological and therefore it has also been called multiple systems organ failure (MSOF). Patients with multiple organ dysfunction syndrome (MODS) make up 10-15% of the intensive care unit population and typically have two to three organ system dysfunctions at time of diagnosis; hypoxia, shock and oliguria are the most common combination. The different components of MODS are: respiratory system, renal system, gastrointestinal system, hepatic system, neurological system, haematology, immunology, and endocrinology and metabolism. No single treatment for MODS can be recommended because it is a maladaptive response to acute severe inflammation and therefore a complication to be prevented rather than a syndrome to treat. Patients with impaired host defence mechanisms are at greatly increased risks of developing sepsis and MODS. Sepsis requires urgent antibiotics and source control with or without surgery.
The inflammatory response is a central component of sepsis as it drives the physiological alterations that are recognized as systemic inflammatory response syndrome (SIRS). In contrast to the hypothesis of exuberant inflammatory response in sepsis is the finding that septic patients may have a relative anti-inflammatory environment. Cellular death may be a key factor in sepsis and its related mortality. Cells that are destined to die can do so by two mechanisms: apoptosis and necrosis. In sepsis, cytokine-induced coagulopathy triggers increased activity of tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) and decreased levels of the natural anticoagulant protein C on mononuclear and endothelial cells. Critical illness related corticosteroid insufficiency (CIRCI) occurs as a result of either a decrease in adrenal steroid production. In patients with severe sepsis, a strategy of glycaemic control using intravenous insulin should include a nutritional protocol with preferential use of the enteral route.