However, in one-third of the patients no primary focus can be found. Multiple organ dysfunction syndrome is well established as the final stage of a continuum: SIRS + infection → sepsis → severe sepsis → Multiple organ dysfunction syndrome.Currently, investigators are looking into genetic targets for possible gene therapy to prevent the progression to multiple organ dysfunction syndrome. Some authors have conjectured that the inactivation of the transcription factors NF-κB and AP-1 would be appropriate targets in preventing sepsis and SIRS. These two genes are pro-inflammatory. However, they are essential components of a normal healthy immune response, so there is risk of increasing vulnerability to infection, which can also cause clinical deterioration. Pathophysiology
A definite explanation has not been found. Local and systemic responses are initiated by tissue damage. Respiratory failure is common in the first 72 hours. Subsequently, one might see liver failure (5–7 days), gastrointestinal bleeding (10–15 days) and kidney failure (11–17 days). Gut hypothesis
The most popular hypothesis by Deitch to explain MODS in critically ill patients is the gut hypothesis. Due to splanchnic hypoperfusion and the subsequent mucosal ischaemia there are structural changes and alterations in cellular function. This results in increased gut permeability, changed immune function of the gut and increased translocation of bacteria. Liver dysfunction leads to toxins escaping into the systemic circulation and activating an immune response. This results in tissue injury and organ dysfunction. Endotoxin macrophage hypothesis
Gram-negative infections in MODS patients are relatively common, hence endotoxins have been advanced as principal mediator in this disorder.
Any object with force and/or speed, typically a ball, fist or vehicle accidents, can result in orbital floor and/or medial wall fractures. These disruptions permit air entry into the orbital subcutaneous from the sinus, with a one-way check valve mechanism that forbids the air from exiting. Victims are often found in sport-related concussion, automobile vehicle accidents, or snowboarding accidents. Traumatic injuries do not cause onset swelling unless there is a forceful injection of air from vigorous sneezing, nose-blowing, or coughing. These generate an acute increase in intraorbital pressure, compromising the intraorbital neurovascular structures, which subsequently trigger the development of orbital emphysema. Postoperative complications
Orbital emphysema is a common result of certain types of surgery, in particular the ones that involve orbital medial wall. It may also occur in other oral, nasal, and maxillofacial surgical interventions, in which the occurrence is unexpected. They can weaken sinuses, bony structure, induce deep orbital tissue damages, or globe perforation that cause air leakage into the periorbital soft tissues and superiorly into the supraorbital fat. These surgical procedures may possibly introduce staphylococci, streptococci, and anaerobic bacteria via a compromised bony wall that can cause periorbital infection. The corresponding weakened or degenerated tissues cannot withstand the sudden increase in intraocular pressure and impaired ocular perfusion, driven by severe coughing or sneezing. It subsequently results in air trapped in the periorbital subcutaneous tissue and the development of orbital emphysema, which is often mistaken as allergic reactions.