[Show abstract][Hide abstract] ABSTRACT: s u m m a r y Donation after cardiac death is defined as organ donation once death is declared after irreversible cessation of circulatory and respiratory functions. The aim of this subjective review is to evaluate the outcome of grafts and recipients in consideration of the length of ischaemia and individuating those who can be considered suitable donors after cardiac arrest. Our main conclusion is that graft and patient survival are comparable either if the organs come from non-heart-beating-donors (NHBD) or heart beating donors (HBD) but complications were reported more frequently in NHBD than in HBD. Warm ischaemia time reduction and close selection of donors are keys to successful NHBD transplantation.
[Show abstract][Hide abstract] ABSTRACT: Sepsis-associated encephalopathy (SAE) is defined as a diffuse or multifocal cerebral dysfunction induced by the systemic response to the infection without clinical or laboratory evidence of direct brain infection.
Its pathogenesis is multifactorial. SAE generally occurs early during severe sepsis and precedes multiple-organ failure.
The most common clinical feature of SAE is the consciousness alteration which ranges from mildly reduced awareness to unresponsiveness and coma.
Diagnosis of SAE is primarily clinical and depends on the exclusion of other possible causes of brain deterioration. Electroencephalography (EEG) is almost sensitive, but it is not specific for SAE. Computed Tomography (CT) head scan generally is negative in case of SAE, while Magnetic Resonance Imaging (MRI) can show brain abnormalities in case of SAE, but they are not specific for this condition. Somatosensitive Evoked Potentials (SEPs) are sensitive markers of developing cerebral dysfunction in sepsis. Cerebrospinal fluid (CBF) analysis is generally normal, a part an inconstant elevation of proteins concentration.
S100B and NSE have been proposed like biomarkers for diagnosis of SAE, but the existing data are controversial. SAE is reversible even if survivors of severe sepsis have often long lasting or irreversible cognitive and behavioral sequel; however the presence of SAE can have a negative influence on survival.
A specific therapy of SAE does not exist and the outcome depends on a prompt and appropriate treatment of sepsis as whole.
[Show abstract][Hide abstract] ABSTRACT: The complex picture of inflammation and coagulation alterations comes to life in acute stroke phases. Increasing evidence points to a strong interaction and extensive crosstalk between the inflammation and coagulation systems: the interest towards this relationship has increased since recent experimental research showed that the early administration of antithrombin III (ATIII) decreases the volume of ischemia in mice and might be neuroprotective, playing an antiinflammatory role.
We aimed to establish the extent of the relationship among markers of inflammation (S100B and IL-18) and procoagulant and fibrinolytic markers (ATIII, thrombin-antithrombin III complex (TAT), Fibrin Degradation Products (FDP), D-dimer) in 13 comatose patients affected by focal cerebral ischemia.
Plasma levels of TAT, D-dimer and FDP, IL18 and S100B were increased. IL-18 and S100B high serum levels in ischemic patients suggest an early activation of the inflammatory cascade in acute ischemic injury.
The basic principles of the interaction between inflammatory and coagulation systems are revised, from the perspective that simultaneous modulation of both coagulation and inflammation, rather than specific therapies aimed at one of these systems could be more successful in stroke therapy.
Neurology International 02/2010; 2(1):e1. DOI:10.4081/ni.2010.e1
[Show abstract][Hide abstract] ABSTRACT: The pathogenesis of sepsis associated encephalopathy (SAE) is not yet clear: the blood-brain barrier (BBB) disruption has been indicated among the possible causative mechanisms. S100B, a calcium binding protein, originates in the central nervous system but it can be also produced by extra-cerebral sources; it is passively released from damaged glial cells and neurons; it has limited passage through the BBB. We aimed to demonstrate BBB damage as part of the pathogenesis of SAE by cerebral spinal fluid (CSF) and serum S100B measurements and by magnetic resonance imaging (MRI). This paper describes four septic patients in whom SAE was clinically evident, who underwent MRI and S100B measurement. We have not found any evidence of CSF-S100B increase. Serum S100B increase was found in three out of four patients. MRI did not identify images attributable to BBB disruption but vasogenic edema, probably caused by an alteration of autoregulation, was diagnosed. S100B does not increase in CSF of septic patients; S100B increase in serum may be due to extracerebral sources and does not prove any injury of BBB. MRI can exclude other cerebral pathologies causing brain dysfunction but is not specific of SAE. BBB damage may be numbered among the contributors of SAE, which aetiology is certainly multifactorial: an interplay between the toxic mediators involved in sepsis and the indirect effects of hyperthermia, hypossia and hypoperfusion.
Neurochemical Research 02/2009; 34(7):1289-92. DOI:10.1007/s11064-008-9907-2 · 2.59 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Global and focal cerebral ischemia is followed by a secondary damage characterized by oxidative stress, excitotoxicity, inflammation and apoptosis. Erythropoietin (EPO) exerts antiapoptotic, anti-inflammatory, antioxidative, angiogenetic and neurotrophic properties. Its potential therapeutic role has been demonstrated in several animal models of cerebral ischemia and also in a clinical trial of ischemic stroke, so it could be considered an ideal compound for neuroprotection in ischemic stroke and in cardiac arrest. Intracerebral hemorrhage (ICH) is the least treatable form of stroke; the mechanisms involved in the secondary brain injury include hematoma mass effect, neuronal apoptosis and necrosis, inflammation. It has been demonstrated in an experimental ICH that EPO intervenes in the inflammatory process, reduces brain water content, hemorrhage volume and hemispheric atrophy, promotes cell survival, preserves cerebral blood flow, has antiapoptotic protective function against oxidative stress and excitotoxic damage. EPO can attenuate acute vasoconstriction and prevent brain ischemic damage in subarachnoid hemorrhage. The neuroprotective function of EPO has been studied also in traumatic brain injury: it reduces the inflammation and improves cognitive and motor deficits. The authors review some of the physiological actions of EPO in the physiopathology of ischemic and hemorrhagic stroke, subarachnoid hemorrhage and brain trauma, and its potential usefulness in the brain injured patient management.
[Show abstract][Hide abstract] ABSTRACT: Sepsis-associated encephalopathy (SAE) is defined as a diffuse cerebral dysfunction induced by the systemic response to infection without any clinical or laboratory evidence of direct infectious involvement of the central nervous system. The astroglial protein S100B has been used as a marker of severity of brain injury and as a prognostic index in trauma patients and cardiac arrest survivors. We measured S100B serum levels in patients with severe sepsis to investigate if the severity of SAE correlated with an increase in S100B levels.
Twenty-one patients, with a diagnosis of severe sepsis, were included in this study. S100B levels were measured at intensive care unit (ICU) admission, 72 h and 7 days after admission. Their association with markers of brain dysfunction such as Glasgow coma scale (GCS), and EEG, and with sepsis-related organ failure assessment score (SOFA) and ICU mortality was investigated.
Fourteen patients had elevated S100B levels. The levels did not correlate with GCS at admission, EEG pattern, or SOFA scores. Also, S100B levels did not differ between patients who recovered neurologically and those who did not (P = 0.62).
In severe sepsis, an increase in S100B does not allow the physicians to distinguish patients with severe impairment of consciousness from those with milder derangements or to prognosticate neurological recovery.
BJA British Journal of Anaesthesia 11/2007; 99(4):518-21. DOI:10.1093/bja/aem201 · 4.85 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: As far as paediatric traumatic brain injury is concerned, it is difficult to quantify the extent of the primary insult, to monitor secondary changes and to predict neurological outcomes by means of the currently used diagnostic tools: physical examination, Glasgow Coma Scale (GCS) score and computed tomography. For this reason, several papers focused on the use of biochemical markers (S100B, neuron-specific enolase) to detect and define the severity of brain damage and predict outcome after traumatic head injury or cardiac arrest.
The aim of this paper is measuring the range of S100B serum concentrations in children affected by traumatic brain injury and describing the possible roles of this protein in the reaction to trauma.
Fifteen children aged 1-15 years were included in the study. Traumatic brain injury severity was defined by paediatric GCS score as mild (9 patients), moderate (2 patients) or severe (4 patients). Blood samples for S100B serum measurement were taken at emergency department admission and after 48 h.
The serum S100B concentration was higher in the group of severe trauma patients, who scored the lowest on the GCS at admission, and among them, the highest values were reported by the children with concomitant peripheral lesions.
The role of S100B in paediatric traumatic brain injury has not been clarified yet, and the interpretation of its increase when the head trauma is associated with other injuries needs the understanding of the physiopathological mechanisms that rule its release in the systemic circulation. The levels of S100B in serum after a brain injury could be related to the mechanical discharge from a destroyed blood-brain barrier, or they could be due to the active expression by the brain, as a part of its involvement in the systemic inflammatory reaction. Early increase of this protein is not a reliable prognostic index of neurological outcome after pediatric traumatic brain injury, since even very elevated values are compatible with a complete neurological recovery.
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to compare serum S100B levels and EEG findings as prognostic indexes in comatose (GCS<8) patients after cardiac arrest.
S100B serum levels were assessed 12 h after the event and EEG findings were recorded within 24 h in comatose cardiac arrest survivors. At hospital discharge, patients were divided into groups according the Glasgow-outcome scale (GOS): group 1 with bad neurological outcome and group 2 with good neurological outcome (GOS 4-5). S100B levels and EEG findings were retrospectively tested about their predictive value.
S100B has a very low specificity (37.5%) while S100B sensitivity is 100%. EEG findings specificity is 75% and sensitivity 50%. S100B was not significantly lower in patients who recovered consciousness (10 patients) and there was no significant difference in EEGs findings between group 1 and 2.
The association of serum S100B levels with EEG might be helpful when used together to formulate outcome in comatose patients within 24 h after cardiac arrest. However, increased levels of S100B 12 h after a cardiac arrest might be expression of a still amendable brain damage.