Sepsis Associated Encephalopathy (SAE)

According to information published by the Mayo Clinic, sepsis has three stages: sepsis, severe sepsis and septic shock. The mortality rate for septic shock is nearly 50 per cent, and an episode of severe sepsis increases the risk of future infections. Severe sepsis causes blood flow to the vital organs, such as the brain, heart and kidneys, to become impaired. Sepsis can also cause blood clots to form in organs and extremities such as arms, legs, fingers and toes, which can lead to organ failure and tissue death (gangrene).

There was a new movie released called Concussion, addressing a neurological deficiency called CTE or chronic traumatic encephalopathy. CTE is quoted as a “degenerative brain condition”, in a Newsweek article titled “CONCUSSION: CAN A WILL SMITH MOVIE CHANGE THE WAY WE LOOK AT FOOTBALL?” This disease was first discovered and diagnosed by Doctor Bennet Omalu, during an autopsy on Mike Webster, legendary former Pittsburgh Steeler.

After many studies, researchers have found that a tremendous amount of football players will develop a brain disease known as chronic traumatic encephalopathy (CTE). This disease is found mostly in athletes who have encountered direct contact to the head. Most of the time, football players will be afflicted with CTE after receiving multiple hits on or near the helmet. Over time, these hits start to affect players in a negative way causing brain trauma, later resulting in CTE. Consequently, CTE has symptoms that are not pleasant and could change players and their families lives forever; some of the symptoms include mood swings and memory loss. CTE also leads to other health afflictions; from the article, Anne McDonnell states, “Brain injuries

The damage then alters the permeability of the axon membrane resulting in a large inflow of calcium, and the release of apoptotic cell death mediators that may be responsible for the phosphorylation, shortening, misfolding and aggregation of tau proteins (2011). Thus, the neurodegeneration that begins in the cortical sulci and initially surrounding only small blood vessels, spreads to larger portions of the brain. This tau-toxic factor associated systemic degeneration in regions of the brain that regulate emotion, memory, and other cognitive functions, leads to the physical and neuropsychological sequelae of CTE (McKee, et al., 2010).

This leads us to the next step in the pathophysiology of Sepsis. Stage 2 of sepsis, which is when SIRS plus the confirmation of an infection has been made. At this stage, the patient’s body has been continuously fighting something in their body and it is starting to have an effect on the patient. Signs and symptoms of sepsis are often nonspecific and include the following: Fever, chills, or rigors, Confusion, Anxiety, Difficulty breathing, Fatigue, malaise, Nausea and vomiting. It is important to identify any potential source of infection. Localizing signs and symptoms referable to organ systems may provide useful clues to the etiology of sepsis and are as follows: Head and neck infections: Severe headache, neck stiffness, altered mental

The impact of TBI on the development of AD is a controversial topic that has caused spirted debate (Jellinger, Paulus, Wroklage, & Litvan, 2001). A study of World War II veterans showed that moderate and severe TBI in early adulthood, that was rated by the duration of the unconscious state or posttraumatic amnesia was associated with increased risk for AD. (Jellinger et al., 2001).

2010). The neuroinflammation is an early, non-specific immune reaction to tissue damage or pathogen invasion (Lee et al. 2010). Inflammation of the central nervous system (CNS) is characterized by increased glial activation, pro-inflammatory cytokine concentration, blood-brain-barrier permeability, and leukocyte invasion (Lee et al. 2010). Microglia are cells that support and protect neuronal functions (Lee at al. 2010). They act as the first and main form of active immune defense that orchestrate the endogenous immune response of the Central Nervous System. The microglia play a central role in the cellular response to pathological lesions such as Aβ. Aβ can attract and activate microglia, leading to clustering of microglia around Aβ deposits sites in the brain (Lee et al. 2010). Even though microglia have neuroprotective functions, neurotoxic mechanisms which involves continuous activation of microglia and toxic factors are released by microglia, which may lead to neuroinflammation (Lee et al. 2010). Astrocytes (star-shaped glial cells) are the most abundant cells in the brain and are located in the brain and spinal. Astrocytes have various functions such as: biochemical support of endothelial cells of the BBB, supplying nutrients to the nervous tissue, maintenance of extracellular ion balance, and healing the brain and spinal cord following traumatic injury (Lee et al., 2010). Chemokines are released by astrocytes which attract microglia and they further express proinflammatory products, thus increasing neuronal damage in the pathogenesis of AD (Lee et al., 2010). Astrocytes play a critical role in Aß clearance and degradation, and they also provide trophic support to neurons forming a protective barrier between Aß deposits and neurons (Wyss-Coray et al., 2003). Neurons contribute to the production of

The word “sepsis” is derived from the ancient Greek word for rotten flesh and putrefaction. Since then, a wide variety of definitions have been applied to sepsis, including sepsis syndrome, severe sepsis, bacteremia, septicemia and septic shock In 1991, the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM) developed a new set of terms and definitions to define sepsis in a more “precise manner” [1, 2]. These definitions take into account the findings that sepsis may result from a multitude of infectious agents and microbial mediators and may not be associated with detectable bloodstream infection. The term “systemic inflammatory response syndrome” (SIRS) was coined to describe the com- mon systemic response to a wide variety of insults. When SIRS was the result of a suspected or confirmed infectious process, it is termed “sepsis”.

Some area’s affected by neuronal loss are the cerebral cortex, the hippocampus, locus coeruleus, and cerebellum. Even with a single TBI, neuronal loss does occur, and evidence suggests this neuronal loss continues beyond the initial injury phase. White matter degeneration does occur as well, and while this study has little information on this, it is noted that white matter injury as well as axonal pathology has been suggested as a mechanism of rapid Aβ genesis. Also seen in neurodegeneration is neuroinflammation that is beyond repair. This inflammation continues after the initial injury in the white matter region, including the corpus callosum. Finally, changes in the cerebellar pathology are noted, in particular loss of cerebellar neurons. Smith, Johnson, & Stewart (2013) note atrophy and demyelination of the folial white matter present in those affected by

When a patient has sepsis early symptoms will include those that define SIRS; abnormal body temperature, increased heart rate, increased respiratory rate, and/or abnormal white blood cell count. If these symptoms are left untreated, organ failure will start to occur. Signs of organ failure can include decreased urine output, sudden changes in mental status, difficulty breathing, decrease in platelets and abnormal heart rhythms. Decreased cardiac output and hypotension may also start to occur, which indicates septic

Acute Necrotizing Encephalopathy is an extremely rare brain disease. The disease is caused secondary to viral infections and can cause a number of life-threatening complications. The disease is caused by a missense mutation in the RANBP2 gene, an important protein that operates within the nuclear pore. The length of both the gene and its resulting products are presented in this poster. It can be caused by a sporadic mutation or can be inherited in an autosomal dominant fashion. No known cure exists, but preventative measures can be taken in order to reduce the chances of developing ANE. In addition, recent findings have helped gained insight into the origins of the disease.

Inflammation is a reaction of tissues in response to any injury the human or vertebrae sustains. Neuroinflammation is the inflammatory response by the glial cells that are present in the nervous system along with neurons. It is an immune response to pathogen invasion or tissue damage most likely to be caused by Infectious bacteria, Traumatic brain injury (TBI), or toxic metabolites. The nervous system contains neurons and glial cells composed of astrocytes, microglia, oligodendrocytes, ependymal cells in the Central nervous system (CNS), and Schwann cells, satellite cells in Peripheral nervous system (PNS). The glial cells are non-neuronal cells that help to form myelin, maintain homeostasis, provide support for neurons with nutrients, destroy

Sepsis is a systemic over response of the immune system, due to an infection that the body tries to fight. This leads to reduced blood flow to vital organs such as the kidneys and the heart, which often results in multiple organ failure with the possibility of death.

Specially, the exposure of brain parenchyma to blood circulation and the release of danger-associated molecule signals from damaged cells that initiate epileptogenic inflammatory cascades. In chronic neuro-inflammation, astrocytes and microglial cells act in a deleterious manner contributing in sustained release of pro-inflammatory cytokines, chemokines (such as S100B, interleukins [i.e., IL-1B,IL-6], tumor necrosis factor-alpha (TNF-a), interferon-y-inducible protein-10 (IP-10)), transforming growth factor (TGF) and proteases. The sensitive reactivation process and the inducible overproduction of pro-inflammatory mediators make astrocyte a very important contributor to the neuro-inflammation in the early onset of brain

Sepsis and Septic Shock have been my personal topic after the life of young Kamil Williams and a 31-year-old Texas man who both contacted a bacterial infection later turn into sepsis. Although I have not formally studied it during my school or university years, I still find the human body, how it can break down and react to certain ailments interesting. The next question would be why does this happen? Well when there is infection or insult upon the body’s immune system normal reacts and causing an inflammatory response. This normally a good thing and it promotes healing and the resolution of the insult, however in Septic Shock the inflammatory response comes explosive and uncontrollable. According to Allison Hotujec, the author of “Severe Sepsis and Septic Shock Protocols,” Sepsis has been called a “malignant intravascular inflammation.” The term malignant is because it is uncontrolled unregulated and self-perpetuating, in the usual immune response here is release of both pro-inflammatory and anti-inflammatory mediators, these balance to promote tissue