Abstract
Sepsis is a major cause of death in intensive care units worldwide. The acute phase of sepsis is often accompanied by sepsis-associated encephalopathy, which is highly associated with increased mortality. Moreover, in the chronic phase, more than 50% of surviving patients suffer from severe and long-term cognitive deficits compromising their daily quality of life and placing an immense burden on primary caregivers. Due to a growing number of sepsis survivors, these long-lasting deficits are increasingly relevant. Despite the high incidence and clinical relevance, the pathomechanisms of acute and chronic stages in sepsis-associated encephalopathy are only incompletely understood, and no specific therapeutic options are yet available. Here, we review the emergence of sepsis-associated encephalopathy from initial clinical presentation to long-term cognitive impairment in sepsis survivors and summarize pathomechanisms potentially contributing to the development of sepsis-associated encephalopathy.
Highlights
Sepsis is a life-threatening and multi-factorial disease with continuously increasing incidence over recent decades from 300 to 1000 sepsis cases per 100,000 people per year in the United States
Even though this study was not designed to investigate the effect of rivastigmine on Sepsis-associated encephalopathy (SAE) patients, these results suggest that cholinesterase inhibitors do not have a beneficial effect in sepsis patients
It should be noted that existence of cerebralabscesses should rather be regarded as infectious encephalitis than as SAE
Summary
Sepsis is a life-threatening and multi-factorial disease with continuously increasing incidence over recent decades from 300 to 1000 sepsis cases per 100,000 people per year in the United States. The overall global incidence is approximately 31 million sepsis cases per year [1,2]. Sepsis-associated encephalopathy (SAE) is one of the most common complications during the acute phase and in later stages after surviving sepsis. It is defined by a diffuse cerebral dysfunction due to the dysregulated host response and absence of a direct central nervous system (CNS) infection. SAE symptoms may already be present before sepsis criteria are fulfilled. From a clinical point of view, the disease course of SAE can be sub-divided into an acute and a chronic phase
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