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Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...

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The encephalopathy in sepsis.

Shidasp Siami1, Djillali Annane, Tarek Sharshar

  • 1General Intensive Care Unit, Raymond Poincaré Teaching Hospital (AP-HP), University of Versailles Saint-Quentin en Yvelines, 104 Boulevard Raymond Poincaré, 92380 Garches, France.

Critical Care Clinics
|February 5, 2008
PubMed
Summary
This summary is machine-generated.

Sepsis can cause severe brain dysfunction, impacting diagnosis and outcomes. Early detection using neurological exams and biomarkers is crucial, though specific treatments remain underdeveloped.

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Area of Science:

  • Neurology
  • Critical Care Medicine
  • Neuroscience

Background:

  • Sepsis-associated encephalopathy (SAE) is a frequent and severe complication of sepsis, with incidence rates from 9% to 71%.
  • SAE significantly increases patient morbidity and mortality.
  • Current diagnosis relies heavily on clinical neurological examination, with symptoms varying from confusion to coma.

Purpose of the Study:

  • To review the current understanding of sepsis-associated encephalopathy.
  • To highlight diagnostic methods and underlying mechanisms.
  • To emphasize the need for targeted therapeutic strategies.

Main Methods:

  • Review of existing literature on sepsis-associated encephalopathy.
  • Analysis of diagnostic tools including neurological examination, electroencephalogram (EEG), somatosensory evoked potentials (SSEPs), and biomarkers like S-100b protein and neuron-specific enolase.
  • Examination of neuroimaging techniques such as Brain MRI for identifying lesions.
  • Discussion of the pathophysiological mechanisms involved in SAE.

Main Results:

  • Neurological examination is the primary diagnostic tool, but objective measures like EEG, SSEPs, and specific biomarkers aid detection.
  • Brain MRI can reveal structural lesions including cerebral infarction, PRES, and leukoencephalopathy.
  • Pathophysiology involves complex inflammatory and non-inflammatory pathways affecting brain cells and the blood-brain barrier.

Conclusions:

  • Sepsis-associated encephalopathy is a critical condition requiring improved diagnostic and therapeutic approaches.
  • While current management focuses on sepsis treatment, specific interventions for SAE are needed.
  • Further research into the mechanisms of SAE is essential for developing targeted therapies.