الفهرس 
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Abstract
Summary
S
epsis is a life-threatening condition due to dysregulation of the body’s response to infection that induces damage to its own tissues and organs. Sepsis- associated brain dysfunction (SABD) is a diffuse dysfunction of the brain that develops in patients with infection, accompanied by a systemic inflammatory response, but without clinical and/or laboratory evidence of direct brain infection. It can present various clinical pictures: inattention, confusion, delirium, excitation, seizures, stupor, and coma. Up to 20% of critically ill patients develop seizures, which can present as convulsive or non-convulsive. An important point is the fact that mortality directly correlates with the severity of SABD. Pediatric patients with SABD warrant attention because the presence of encephalopathy with sepsis increases the mortality to 50% as compared to 26% in non-encephalopathic patients.
This case-control study included 61 pediatric patients, all of them were previously healthy, presented to Pediatric Intensive Care Unit, Children’s hospital, Ain Shams University who were chosen after consideration of inclusion and exclusion criteria. The included patients were further subdivided to three groups, according to pSOFA score, as follows: 20 patients with sepsis, 21 patients with septic shock and 20 patients with no sepsis or septic shock, as controls.
Bedside full history and detailed clinical examination, functional echocardiography including (cardiac index and systemic vascular resistive index), transcranial doppler ultrasound parameters including (pulsatility index, resistive index, mVMCA, cerebral blood flow index and Cerebral vasomotor reactivity), EEG recording for the predominant brain electrical activity, and the following laboratory investigation were performed: CBC, CRP, liver and kidney function tests, blood gases, and serum lactate.
The age of patients ranged from 1-60 months with mean age 8.9 (±9) months. The primary causes of sepsis and septic shock were pulmonary diseases in 43.4% of patients, while extra-pulmonary diseases compromised 56.6% of cases.
The overall mortality among the studied patients was 32.7% (5 patients from the septic shock group died during the time interval of the study and didn’t complete the study, while the 28-days mortality included 3 patients from sepsis group and 12 patients from the septic shock group). Mortality rates were statistically significantly higher in patients with sepsis and septic shock compared to control group.
The need for vasopressors and inotropic supports was higher among patients with septic shock (n= 9/21), compared with sepsis group (n= 0/20) and control group (n= 0/20).
In our study, most patients showed a high PI at some point during enrolment. Given that increased PI is associated with increased cerebral resistance, we suspect that most patients showed cerebral microcirculation impairment. Also, patients with high PI showed a lower mean mVMCA and CBFi compared with patients with lower PI. This finding potentially resulting in a decrease in CBF in these patients.
In our study, we found that cerebral vasomotor reactivity evidenced by CO2 reactivity was significantly disturbed at hour 24-48 of enrolment in septic shock patients compared to control patients.
During our study, we found that patients with septic shock experienced different EEG patterns, with excessive theta waves were the most prominent pattern change in the first 24-48 hours. This was followed by burst suppression pattern at hour 72.
Pulsatility index and Resistive index were higher among septic shock patients with SABD compared to those without SABD along the whole-time interval of the study. On the other hand, the mean velocity in MCA was lower among septic shock patients with SABD compared to those without SABD along the whole-time interval of the study.
Cerebral blood flow index showed an initial decline in the first 24 hours of enrolment in both septic shock patients without SABD and those with SABD, followed by an increase in those without SABD till the end of the study. On the other hand, a noticeable decline in the CBFi in those with SABD was noted during the second day of enrolment, followed by a slight increase on the last day of enrolment.
Regarding cerebral vasomotor reactivity (cerebral autoregulation), we noticed a remarkable decline in septic shock group with SABD starting from hour 24 of enrolment till the end of the study.
In our study, we found that triphasic waves and burst suppression were only recorded in patients with SABD. Mortality among patients with burst suppression were 100%.