Showing papers by "Clinical Emergency Hospital Bucharest published in 2009"

Cardiac dysfunctions following spinal cord injury

Abstract: The aim of this article is to analyze cardiac dysfunctions occurring after spinal cord injury (SCI). Cardiac dysfunctions are common complications following SCI. Cardiovascular disturbances are the leading causes of morbidity and mortality in both acute and chronic stages of SCI. We reviewed epidemiology of cardiac disturbances after SCI, and neuroanatomy and pathophysiology of autonomic nervous system, sympathetic and parasympathetic. SCI causes disruption of descendent pathways from central control centers to spinal sympathetic neurons, originating into intermediolateral nuclei of T1-L2 spinal cord segments. Loss of supraspinal control over sympathetic nervous system results in reduced overall sympathetic activity below the level of injury and unopposed parasympathetic outflow through intact vagal nerve. SCI associates significant cardiac dysfunction. Impairment of autonomic nervous control system, mostly in patients with cervical or high thoracic SCI, causes cardiac dysrrhythmias, especially bradycardia and, rarely, cardiac arrest, or tachyarrhytmias and hypotension. Specific complication dependent on the period of time after trauma like spinal shock and autonomic dysreflexia are also reviewed. Spinal shock occurs during the acute phase following SCI and is a transitory suspension of function and reflexes below the level of the injury. Neurogenic shock, part of spinal shock, consists of severe bradycardia and hypotension. Autonomic dysreflexia appears during the chronic phase, after spinal shock resolution, and it is a life-threatening syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with SCI above the splanchnic sympathetic outflow (T5-T6). Besides all this, additional cardiac complications, such as cardiac deconditioning and coronary heart disease may also occur. Proper prophylaxis, including nonpharmacologic and pharmacological strategies and cardiac rehabilitation diminish occurrence of the cardiac dysfunction following SCI. Each type of cardiac disturbance requires specific treatment.

Genetics of craniosynostosis: review of the literature.

Abstract: Craniosynostosis represents a defection of the skull caused by early fusion of one or more cranial sutures. The shape alteration of the cranial vault varies, depending on the fused sutures, so that compensatory growth occurs in dimensions not restricted by sutures. Craniosynostosis can be divided into two main groups: syndromic and nonsyndromic. Nonsyndromic craniosynostosis is typically an isolated finding that is classified according to the suture(s) involved. Syndromic craniosynostosis is associated with various dysmorphisms involving the face, skeleton, nervous system and is usually accompanied by developmental delay. In the last 15 years, research on craniosynostosis has progressed from the description of gross abnormalities to the understanding of the genetic basis of certain cranial deformities. Mutations in the genes encoding fibroblast growth factor receptors 1, 2 and 3 (FGFR-1, FGFR-2, FGFR-3), TWIST and MSX2 (muscle segment homebox 2) have been identified in certain syndromic craniosynostosis. The molecular basis of many types of syndromic craniosynostosis is known and diagnostic testing strategies will often lead to a specific diagnosis. Although the clarification of a genetic lesion does not have a direct impact on the management of the patient in many cases, there is a significant benefit in providing accurate prenatal diagnosis. This review summarizes the available knowledge on cranisynostosis and presents a graduated strategy for the genetic diagnosis of these craniofacial defects.

Efficacy and safety of tigecycline versus levofloxacin for community-acquired pneumonia

Abstract: Tigecycline, an expanded broad-spectrum glycylcycline, exhibits in vitro activity against many common pathogens associated with community-acquired pneumonia (CAP), as well as penetration into lung tissues that suggests effectiveness in hospitalized CAP patients. The aim of the present study was to compare the efficacy and safety of intravenous (IV) tigecycline with IV levofloxacin in hospitalized adults with CAP. In this prospective, double-blind, non-inferiority phase 3 trial, eligible patients with a clinical diagnosis of CAP supported by radiographic evidence were stratified by Fine Pneumonia Severity Index and randomized to tigecycline or levofloxacin for 7-14 days of therapy. Co-primary efficacy endpoints were clinical response in the clinically evaluable (CE) and clinical modified intent-to-treat (c-mITT) populations at test-of-cure (Day 10-21 post-therapy). Of the 428 patients who received at least one dose of study drug, 79% had CAP of mild-moderate severity according to their Fine score. Clinical cure rates for the CE population were 88.9% for tigecycline and 85.3% for levofloxacin. Corresponding c-mITT population rates were 83.7% and 81.5%, respectively. Eradication rates for Streptococcus pneumoniae were 92% for tigecycline and 89% for levofloxacin. Nausea, vomiting, and diarrhoea were the most frequently reported adverse events. Rates of premature discontinuation of study drug or study withdrawal because of any adverse event were similar for both study drugs. These findings suggest that IV tigecycline is non-inferior to IV levofloxacin and is generally well-tolerated in the treatment of hospitalized adults with CAP. NCT00081575

A life threatening problem in infants: supratentorial epidural hematoma

Abstract: EDH in infants represents a life–threatening complication of head injury, which requires early identification and prompt surgical or conservative management depending on the patient's clinical condition, the size of EDH, and the presence of a midline structure shift on the head's CT scan.

The prognostic value of blood glucose level on admission in non-diabetic patients with acute myocardial infarction.

Abstract: UNLABELLED The diabetic patients represent a population with a high risk of morbidity and mortality because of vascular complications. Out of them, all the patients with acute ST-elevation myocardial infarction have a more reserved prognostic than those without diabetes mellitus. Moreover, the patients with impaired glucose tolerance have a more severe evolution in case of a myocardial infarction. AIM We wondered about the progress of patients with myocardial infarction and high blood glucose levels in admittance who had not been previously diagnosed with diabetes mellitus. MATERIALS AND METHODS We took 128 patients (who did not have diabetes) with acute ST-elevation myocardial infarction and divided them into three groups, according to the blood glucose level in admittance ( 200 mg/dL); we also analyzed a group of diabetics with acute myocardial infarction who were admitted in the same period in our clinic. We made a prospective analysis over a period of 30 days. We evaluated the mortality at 30 days (as primary objective), as well as the extent of the infarction and the change of the left ventricle systolic function (secondary objectives). RESULTS Both mortality and the mass of myocardial necrosis grew relative to the blood glucose level in admittance; instead, the ejection fraction varied inversely to the initial blood glucose level. CONCLUSION The admittance blood glucose level represents a useful and available marker for the initial stratification of risks in patients with acute myocardial infarction, even in those undiagnosed with diabetes mellitus.