الفهرس 
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Abstract
Sepsis commonly produces brain dysfunction known as sepsis-associated encephalopathy, which can vary from a transient, reversible encephalopathy to irreversible brain damage. Sepsis associated encephalopathy has been recorded in over 50% of patients presenting with sepsis. As well as being one of the commonest causes of delirium in critically ill patients, sepsis associated encephalopathy (SAE) has been found to be an independent prognostic factor for increased mortality. In addition, SAE has been associated with detrimental long term cognitive impairment in those who survive an episode of sepsis.
To date, the exact pathogensis of SAE remains unclear; alteration in cerebral perfusion during sepsis has been found to play a possible role in the development of this clinical entity. Microcirculatory dysfunction and dissociation between cerebral cells’ needs and perfusion at several cerebral areas was found in expermental sepsis models.
Magnesium sulphate has been shown to have a protective effect on BBB integrity in multiple experimental models. Other studies have also documented the vasodilatory effect of magnesium sulfate on the smaller-diameter intracranial vessels distal to the middle cerebral artery, thereby relieving cerebral ischemia.
Our study aimed at studying the effect of the administration of magnesium sulphate on the flow velocities in the middle cerebral artery of patients presenting with sepsis associated encephalopathy, and the relationship between these findings with the neurological outcome of these patients.
The study was conducted on 46 adult patients admitted to the ICU during the first 24 hours of the of the onset of sepsis and/ or septic shock, with a positive CAM-ICU score and a GCS <15. The patients were divided into 2 groups, with one group receiving an intravenous bolus dose of 6 g magnesium sulphate along with the standard management of sepsis, and the other group receiving the standard management of sepsis and septic shock only.