Values of blood copeptin level as a marker of unfavorable forecast in subarachnoid haemorrhage of the brain of atraumatic origin

Objective – to evaluate of diagnostic informativeness of сopeptin serum values in determining the risk of complications in patients with subarachnoid hemorrhage.Materials and methods. A prospective cohort study of 82 patients (40 men and 42 women) with spontaneous (non-traumatic) subarachnoid hemorrhage (SAH) from the age of 23 to 72 years (average age – (49,6 ±1,3) year) was conducted.Results. Complications were recorded in 31 (74.20 %) patients with a serum level of copeptin ≥ 0.605 ng/ml on the third day of the SAH, which was in 9.49 times higher (95 % CI 3.60–24.80, р ˂0.0001) than in patients with a serum level of copeptin < 0.605 ng/ml. When determining the cumulative risk of developing complications of SAH, the values ​​of positive and negative predictive values ​​of serum levels of copeptin on third day of SAH were 74.19 % and 92.20 % respectively, the accuracy of prediction (the sum of correctly classified observations) was 85.39 %.Conclusions. ROC-analysis suggests that the serum level of copeptin on third day of SAH ≥ 0.605 ng/ml is characterized by an optimal ratio of sensitivity and specificity in assessing the cumulative risk of developing such SAH complications as secondary ischemia combined with cerebral angiospasm.

Proposed Definition of Experimental Secondary Ischemia for Mouse Subarachnoid Hemorrhage

Inconsistency in outcome parameters for delayed cerebral ischemia (DCI) makes it difficult to compare results between mouse studies, in the same way inconsistency in outcome parameters in human studies has for long obstructed adequate comparison. The absence of an established definition may in part be responsible for the failed translational results. The present article proposes a standardized definition for DCI in experimental mouse models, which can be used as outcome measure in future animal studies. We used a consensus-building approach to propose a definition for “experimental secondary ischemia” (ESI) in experimental mouse subarachnoid hemorrhage that can be used as an outcome measure in preclinical studies. We propose that the outcome measure should be as follows: occurrence of focal neurological impairment or a general neurological impairment compared with a control group and that neurological impairment should occur secondarily following subarachnoid hemorrhage (SAH) induction compared with an initial assessment following SAH induction. ESI should not be used if the condition can be explained by general anesthesia or if other means of assessments sufficiently explain function impairment. If neurological impairment cannot reliably be evaluated, due to scientific setup. Verification of a significant secondary impairment of the cerebral perfusion compared with a control group is mandatory. This requires longitudinal examination in the same animal. The primary aim is that ESI should be distinguished from intervention-related ischemia or neurological deficits, in order establish a uniform definition for experimental SAH in mice that is in alignment with outcome measures in human studies.

POSSIBILITIES OF MATHEMATICAL DEFINITION OF UNFAVOURABLE COURSE OF SUBARACHNOID HAEMORRHAGE IN THE ACUTE PERIOD

Subarachnoid haemorrhage (SAH) is associated with a 30-day mortality rate of 50% and is one of the most life-threatening cerebrovascular diseases. Objective. Toevaluatetheprognosticsignificance and informativeness of some clinical indicators, highlighting the most optimal and reliable potential factors in the development of a mathematical equation for calculating the personal probability of complications in patients with subarachnoid hemorrhage of atraumatic etiology. Materials and methods. A clinical experimental study involved 87 patients with SAH, 44 were men, 43 – women. On the first day after SAH, half of the patients were hospitalized – 46 people (52,87%). Results. The constructed model for calculating the probability of events such as secondary ischemia, hydrocephalus, or cerebral vasospasm over the next 14 days indicates the correctness and adequacy of the constructed model of logistic regression.The personal probability of a complication is calculated by the formula: p = 1 / (1 + e-z), where p is the % probability of a complication of SAH; z = –45,5 + 17,5* Copeptine –0.44 × Na + 0,06 × Age + 1,99 × Ball (Hunt-Hess). Conclusions. The prognostic model allows us to consider that secondary ischemia and cerebral vasospasm are not only predictors of poor prognosis and potential factors for the formation of complications, but also are indicators for the correct determination of individual cumulative risk in SAH. Keywords: notraumatic hemorrhage, C. S. Ogilvy, copeptin, SIADH syndrome, hyponatremia, prognosis, logistic regression.

SNAKE BITE OF A DIAMONDBACK RATTLESNAKE - CLINICAL CASE AND MANAGEMENT

Rattlesnake envenomation incidence and its severity remain largely misunderstood in Europe. The evolution of cases reported in the few countries, where these accidents are correctly reported, proves to be unpredictable. Rattlesnake venom is mainly hemotoxic, affecting mainly the blood vessels, blood cells and the heart. The venom contains zinc metalloproteinases, cytotoxins and myotoxins. As an additional effect, the necrosis of skeleton muscles is produced by the venom through secondary ischemia and reduced perfusion. We will present the case of a 30-year-old lady, snake and tarantula breeder from Bucharest, presented at the emergency department on the 15Th of March 2015 after one of her pets, a diamondback rattlesnake had bitten her wrist.

Two clinical cases of nonspecific aortoarteritis

Non-specific aortoarteritis is a chronic inflammatory disease of the aorta and its main branches with the stenosis or occlusion development of the affected blood vessels and secondary ischemia of organs and tissues. The main clinical symptoms most often are pulselessness or low-tension pulse on one of hands, the asymmetry of brachial artery systolic blood pressure, intermittent claudication, weakness, weight loss. Non-specific aortoarteritis is an uncommon condition for general practitioners, and the disease manifestations are often interpreted as symptoms of another pathology. It causes large number of diagnostic and tactical mistakes in management of these patients. The relative rarity of nonspecific aortoarteritis becomes one of the factors determining the complexity and time lag of its diagnosis, inadequate treatment, what leads to early disability and high risk of life-threatening complications development. The article considers two clinical cases of non-specific aortoarteritis. In one of them abdominal pain syndrome is on the foreground, in the other - cephalalgia. Often clinicians consider given symptoms in young people as a manifestation of dyspepsia (in the first patient) and one of the vasoneurosis symptoms (in the second one). The difficulty in diagnosis is that there is no specific laboratory and instrumental symptoms which are pathognomonic for nonspecific aortoarteritis as in other vasculitis.

The Endothelium, A Protagonist in the Pathophysiology of Critical Illness: Focus on Cellular Markers

The endotheliumis key in the pathophysiology of numerous diseases as a result of its precarious function in the regulation of tissue homeostasis. Therefore, its clinical evaluation providing diagnostic and prognostic markers, as well as its role as a therapeutic target, is the focus of intense research in patientswith severe illnesses. In the critically ill with sepsis and acute brain injury, the endothelium has a cardinal function in the development of organ failure and secondary ischemia, respectively. Cellular markers of endothelial function such as endothelial progenitor cells (EPC) and endothelialmicroparticles (EMP) are gaining interest as biomarkers due to their accessibility, although the lack of standardization of EPC and EMP detection remains a drawback for their routine clinical use. In this paper we will review data available on EPC, as a general marker of endothelial repair, and EMP as an equivalent of damage in critical illnesses, in particular sepsis and acute brain injury. Their determination has resulted in new insights into endothelial dysfunction in the critically ill. It remains speculative whether their determination might guide therapy in these devastating acute disorders in the near future.