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Sepsis Associated Encephalopathy.

Chaudhry N, Duggal AK - Adv Med (2014)

Bottom Line: The evaluation of cognitive dysfunction is made difficult by the absence of any specific investigations or biomarkers and the common use of sedation in critically ill patients.SAE thus remains diagnosis of exclusion which can only be made after ruling out other causes of altered mentation in a febrile, critically ill patient by appropriate investigations.In spite of high mortality rate, management of SAE is limited to treatment of the underlying infection and symptomatic treatment for delirium and seizures.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Academic Block, G.B. Pant Hospital, New Delhi 110002, India.

ABSTRACT
Sepsis associated encephalopathy (SAE) is a common but poorly understood neurological complication of sepsis. It is characterized by diffuse brain dysfunction secondary to infection elsewhere in the body without overt CNS infection. The pathophysiology of SAE is complex and multifactorial including a number of intertwined mechanisms such as vascular damage, endothelial activation, breakdown of the blood brain barrier, altered brain signaling, brain inflammation, and apoptosis. Clinical presentation of SAE may range from mild symptoms such as malaise and concentration deficits to deep coma. The evaluation of cognitive dysfunction is made difficult by the absence of any specific investigations or biomarkers and the common use of sedation in critically ill patients. SAE thus remains diagnosis of exclusion which can only be made after ruling out other causes of altered mentation in a febrile, critically ill patient by appropriate investigations. In spite of high mortality rate, management of SAE is limited to treatment of the underlying infection and symptomatic treatment for delirium and seizures. It is important to be aware of this condition because SAE may present in early stages of sepsis, even before the diagnostic criteria for sepsis can be met. This review discusses the diagnostic approach to patients with SAE along with its epidemiology, pathophysiology, clinical presentation, and differential diagnosis.

No MeSH data available.


Related in: MedlinePlus

Algorithm for diagnosis of sepsis associated encephalopathy. RASS: Richmond Agitation-Sedation Scale, FOUR: Full Outline of Unresponsiveness, GCS: Glasgow coma scale, SEP: somatosensory evoked potentials, NSE: neuron specific enolase, CAM/CAM-ICU: Confusion Assessment Method (Intensive Care Unit), and ATICE: Assessment to Intensive Care Environment.
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fig2: Algorithm for diagnosis of sepsis associated encephalopathy. RASS: Richmond Agitation-Sedation Scale, FOUR: Full Outline of Unresponsiveness, GCS: Glasgow coma scale, SEP: somatosensory evoked potentials, NSE: neuron specific enolase, CAM/CAM-ICU: Confusion Assessment Method (Intensive Care Unit), and ATICE: Assessment to Intensive Care Environment.

Mentions: SAE is a diagnosis of exclusion and requires the exclusion of direct infection of the central nervous system, multisystem organ failure, head trauma, fat embolism, and drugs side effects. The first step in evaluation of suspected SAE would be to assess the mental status and identify features of encephalopathy which could be subtle particularly in early stages and can be confounded by the common use of sedatives in this population. The next step is to investigate and eliminate the possibility of a primary CNS pathology that may be responsible for an altered level of consciousness. Last but not least, evaluation should be aimed at identifying the source of infection and the responsible infectious agent (Figure 2).


Sepsis Associated Encephalopathy.

Chaudhry N, Duggal AK - Adv Med (2014)

Algorithm for diagnosis of sepsis associated encephalopathy. RASS: Richmond Agitation-Sedation Scale, FOUR: Full Outline of Unresponsiveness, GCS: Glasgow coma scale, SEP: somatosensory evoked potentials, NSE: neuron specific enolase, CAM/CAM-ICU: Confusion Assessment Method (Intensive Care Unit), and ATICE: Assessment to Intensive Care Environment.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4590973&req=5

fig2: Algorithm for diagnosis of sepsis associated encephalopathy. RASS: Richmond Agitation-Sedation Scale, FOUR: Full Outline of Unresponsiveness, GCS: Glasgow coma scale, SEP: somatosensory evoked potentials, NSE: neuron specific enolase, CAM/CAM-ICU: Confusion Assessment Method (Intensive Care Unit), and ATICE: Assessment to Intensive Care Environment.
Mentions: SAE is a diagnosis of exclusion and requires the exclusion of direct infection of the central nervous system, multisystem organ failure, head trauma, fat embolism, and drugs side effects. The first step in evaluation of suspected SAE would be to assess the mental status and identify features of encephalopathy which could be subtle particularly in early stages and can be confounded by the common use of sedatives in this population. The next step is to investigate and eliminate the possibility of a primary CNS pathology that may be responsible for an altered level of consciousness. Last but not least, evaluation should be aimed at identifying the source of infection and the responsible infectious agent (Figure 2).

Bottom Line: The evaluation of cognitive dysfunction is made difficult by the absence of any specific investigations or biomarkers and the common use of sedation in critically ill patients.SAE thus remains diagnosis of exclusion which can only be made after ruling out other causes of altered mentation in a febrile, critically ill patient by appropriate investigations.In spite of high mortality rate, management of SAE is limited to treatment of the underlying infection and symptomatic treatment for delirium and seizures.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Academic Block, G.B. Pant Hospital, New Delhi 110002, India.

ABSTRACT
Sepsis associated encephalopathy (SAE) is a common but poorly understood neurological complication of sepsis. It is characterized by diffuse brain dysfunction secondary to infection elsewhere in the body without overt CNS infection. The pathophysiology of SAE is complex and multifactorial including a number of intertwined mechanisms such as vascular damage, endothelial activation, breakdown of the blood brain barrier, altered brain signaling, brain inflammation, and apoptosis. Clinical presentation of SAE may range from mild symptoms such as malaise and concentration deficits to deep coma. The evaluation of cognitive dysfunction is made difficult by the absence of any specific investigations or biomarkers and the common use of sedation in critically ill patients. SAE thus remains diagnosis of exclusion which can only be made after ruling out other causes of altered mentation in a febrile, critically ill patient by appropriate investigations. In spite of high mortality rate, management of SAE is limited to treatment of the underlying infection and symptomatic treatment for delirium and seizures. It is important to be aware of this condition because SAE may present in early stages of sepsis, even before the diagnostic criteria for sepsis can be met. This review discusses the diagnostic approach to patients with SAE along with its epidemiology, pathophysiology, clinical presentation, and differential diagnosis.

No MeSH data available.


Related in: MedlinePlus