Introduction: The widespread use of sevoflurane as an induction and maintenance volatile agent of general anesthesia demostrates an increased safety profile. Sevoflurane contact with CO2 absorbents lead to the occurrence of toxic compounds such as Compund A and Compound B. Among the side efffects of Sevoflurane remember the renal toxic effect much discussed in the literature but still unresolved. In previous research we have demonstrated the glomerular protein changes as a result of exposure to Sevoflurane. In the current study we intend to monitor the changes in blood urea nitrogen and serum creatinine after exposure to Sevoflurane.
Material and method: We included in our study 90 patients who were anesthetized in the Department of Anesthesiology of the County Mure Hospital during 01.10.2009-01.10.2014. They had normal values for blood urea nitrogen and serum creatinine and had no preoperative proteinuria. Serum and urine samples were taken preoperatively and at 24 and 72 hours postanesthetic and were analyzed in the laboratory. Proteinuria was determined by spectrophotometry.
Results: After protein quantitative determination by spectrophotometry and statistical anaysis we obtained significant differences by comparing the average preoperative/24 hours total protein (p<0.0001) and 24/72 hours (p<0.0001). There are no significant statistical differences by comparing the blood urea nitrogen at the three intervals (p<0.53) and no statistical changes for mean serum creatinine (p<0.18).
Conclusions: Changes in glomerular filtered proteins following exposure to Sevoflurane demonstrate its toxic effect on glomerular tubules. Lack of perioperative significant wich is why we recommend determining perioperative urinary protein as a marker of glomerular damage.
The aim of this work was to study for the first time in Romania Insertion/Deletion (I/D) polymorphism of the Vascular Endothelial Growth Factor (VEGF) gene in a group of patients with established type 2 diabetes mellitus (DM) and diabetic peripheral neuropathy (DPN) compared with a control group.
This was a case-control study consisting of a group of 84 patients with type 2 DM and DPN, diagnosed by clinical neurological examination and electrophysiological nerve conduction studies and a control group of 90 healthy volunteers. For deoxyribonucleic acid (DNA) isolation, a DNA purification kit from Zymo Research was used. In vitro amplification of DNA sequences was achieved by polymerase chain reaction (PCR). Selective in vitro amplification of a DNA fragment of known sequence is based on the principle of extension of a primer (“primer and PCR amplicon”). DNA fragments were separated by gel electrophoresis. For proper viewing and interpreting of agarose gels Vilber Lourmat system was used. D allele frequency of VEGF was significantly higher in patients with diabetic peripheral neuropathy (53.57%) compared with controls (25%), p=0.0001.
There is a positive association between I/D polymorphism of VEGF gene and the presence of diabetic peripheral polyneuropathy. Our study suggests that D allele of VEGF gene is a risk factor for the occurrence of DPN.
There are rare reports of the occurrence of acute transverse myelitis and Guillain–Barré syndrome after various surgical procedures and general/epidural anaesthesia. The concomitant occurrence of these pathologies is very rare and is called Guillain–Barré and acute transverse myelitis overlap syndrome. In this article, we present the case of a second trimester pregnant patient who developed Guillain–Barré and acute transverse myelitis overlap syndrome.
We report the case of a 16-year-old female patient who underwent a therapeutic termination of pregnancy two weeks prior to the onset of the disease with gradual development of a motor deficit with walking and sensitivity disorders, fecal incontinence. The diagnosis was based on clinical exam, electroneurography and spinal magnetic resonance imaging. Endocrinopathies, infectious diseases, autoimmune and inflammatory diseases, neoplastic diseases and vitamin deficiencies were ruled out. Our patient attended five sessions of therapeutic plasma exchange, followed by steroid treatment, intravenous immunoglobulin with minimum recovery of the motor deficit in the upper limbs, but without significant evolution of the motor deficit in the lower limbs. The patient was discharged on maintenance corticotherapy and immunosuppressive treatment with azathioprine.
We report a very rare association between Guillain–Barré syndrome and acute transverse myelitis triggered by a surgical intervention with general anaesthesia. The overlap of Guillain–Barré syndrome and acute transverse myelitis makes the prognosis for recovery worse, and further studies are needed to establish the first-line therapy in these cases.
Cardiovascular autonomic neuropathy is the most frequent clinical form of autonomous diabetic neuropathy and appears secondary to cardiac autonomous fibre involvement, actively involved in cardiac rhythm impairment. Type 2 diabetes mellitus patients can present cardiac autonomic neuropathy early in the disease. Autonomous nerve function in DM patients should be assessed as early as the diagnosis is set in order to establish the optimal therapeutic strategy. The most frequent cardio-vagal test used is heart rate variability. An abnormal heart rate variability in the presence of orthostatic arterial hypotension indicates a severe cardiac autonomic neuropathy diagnosis. The development of cardiac autonomic neuropathy is subjected to glycaemic control, duration of the disease and associated risk factors. The glycaemic control is extremely important, especially early in the disease. Therefore, a poor glycaemic control carries unfavourable long-term effects, despite an ulterior optimal control, a phenomenon named “hyperglycaemic memory”. In type 2 diabetes mellitus patients, the association of cardiac autonomic neuropathy with intensive glycaemic control increases the mortality rate, due to the fact, that, secondary to autonomous impairment, the patients do not present the typical symptoms associated with hypoglycaemia. Stratifying the cardiac autonomic neuropathy aids the clinician in assessing the morbidity and mortality risk of diabetes mellitus patients, because it is an independent risk factor for mortality, associated with silent myocardial infarctions and the risk of sudden death.
A free-floating carotid artery thrombus is a very rare ultrasonographical finding in patients with acute ischemic cerebrovascular events. One of the main causes of this presentation is represented by the hypercoagulability status of the patients. We report the case of a young male patient who presented with several transient ischaemic attacks secondary to a mobile thrombus in the left carotid sinus. Two hematological abnormalities, essential thrombocytosis and methylene tetrahydrofolate reductase mutation were found to be related to the thrombus formation. The role of the latter in the pathogenesis of ischemic stroke is not well documented in the literature. Following antiplatelet and anticoagulant medication, there was a fast dissolution of the thrombus, followed by a favorable clinical outcome. Neurologists should be aware that young patients with stroke require extensive imagistic and laboratory screening for an accurate etiological diagnosis.
The processes of demyelination and neurodegeneration in the central nervous system (CNS) of multiple sclerosis (MS) patients and experimental autoimmune encephalomyelitis (EAE) are secondary to numerous pathophysiological mechanisms. One of the main cellular players is the Th17 lymphocyte. One of the major functions described for Th17 cells is the upregulation of pro-inflammatory cytokines, such as IL-17 at the level of peripheral and CNS inflammation. This review will focus on the newly described and unexpected, direct role played by the Th17 cells in the CNS of MS patients and EAE models. Th17 and their main cytokine, IL-17, are actively involved in the onset and maintenance of the immune cascade in the CNS compartment as Th17 were found to achieve brain-homing potential. Direct interaction of myelin oligodendrocyte glycoprotein - specific Th17 with the neuronal cells firstly induces demyelination and secondly, extensive axonal damage. The Th17 cells promote an inflammatory B cell response beyond the BBB through the presence of infiltrating Th follicles. Due to their role in preventing remyelination and direct neurotoxic effect, Th17 cells might stand for an important connection between neuroinflammation and neurodegeneration in a devastating disease like MS. The Th17 cell populations have different mechanisms of provoking an autoimmune attack not only in the periphery but also in the CNS of MS patients.
Tay-Sachs disease (TSD) is a rare, inherited, autosomal rececessive lysosomal storage disease. The late-onset form is an uncommon condition among non-Jewish population.
We present the case of a 32 years old male patient without Jewish origins, in whom the disease began in adolescence and was initially diagnosed with spinal muscular atrophy. He developed progressively protean neurological symptomatology, including tetraparesis, cerebellar and extrapyramidal syndromes. The diagnosis was based on the cerebral MRI, showing severe cerebellar atrophy and the determination of the Hexosaminidase A activity, revealing low level.
In patients showing signs of lower motor neuron involvement, cerebellar and pyramidal signs and marked cerebellar atrophy the late-onset TSD should be suspected, and the first step in establishing the diagnosis should be to determine the serum activity of Hexosaminidase A.
Traumatic bilateral dissection of the carotid arteries is a rare condition with potentially life-threatening complications. The case of a 57-year-old male patient with acute onset left sided hemiparesis, twelve hours after a blunt head injury, caused by a horse kick, is reported. A cerebral CT scan revealed right middle cerebral artery (MCA) territory infarction. Based on Duplex ultrasound and Angio CT scan findings, a diagnosis of bilateral ICA dissection was established. Despite antithrombotic treatment, the patient presented with a progressive worsening of his neurological status. The control CT scan evidenced malignant right MCA territory infarction that required decompressive craniotomy. The patient was discharged with significant neurological deficits. Together with this case, the aetiologies, clinical manifestations, diagnostic and therapeutical options and outcome of carotid artery dissection are discussed.
Introduction: Lesions of the carotid and vertebral arteries secondary to direct trauma, called blunt cerebrovascular injuries (BCVI) are relatively rare and are markedly different from spontaneous dissections. Ischaemic stroke is a significant complication, with high morbidity and mortality rates. The basis of a diagnosis relies on appropriate, high sensitivity imaging screening.
Case report: We present the case of a 31 years old male patient with polytraumatism secondary to a motor vehicle accident, who was admitted to an orthopaedic clinic for multiple lower extremity fractures. His fractures were treated surgically. He developed in the 3rd day after the admission left sided hemiparesis secondary to ischaemic stroke. The diagnosis of traumatic carotid artery injury (TCAI) was based on duplex ultrasound and angio CT scans. The outcome was favourable despite the severe carotid lesions presenting with occlusion secondary to dissection.
Conclusions: In the majority of BCVI cases there is a variable latent period between the time of injury and the development of stroke. The management of cases is challenging because in the majority of cases there are multiple associated injuries. Although antithrombotics are widely used in the treatment, there is no consensus regarding the type of agent, the optimal dose or treatment duration.