Grazing-incidence diffraction from multilayers.
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Biomedical subjects
Publications and source records attributed to S Tixier.
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A number of severe rhabdomyolysis with acute renal failure have been reported following spine surgery in knee chest position. CPK were measured postoperatively in 93 patients (A group), comparatively with two groups in which respectively neurosurgery without any muscle stretching (B group) and abdominal surgery with aid of retractors (C group) were performed. CPK were significantly and similarly increased in A and C groups only. This postoperative increase of CPK appears to be related more to the muscle stretching than to the posture itself. Intraoperative low blood pressure and an operating time longer than 4 hrs contribute probably to rhabdomyolysis. No renal failure was observed in our series. Low limb vascular insufficiency is the main contra-indication of knee chest position. Postoperative diuresis surveillance is mandatory in all cases, CPK analysis is not.
Bolus injections of lidocaine are commonly used during neuroanesthesia to prevent or treat ICP elevations caused by tracheal or painful stimuli. Lidocaine can also be employed in case of hard intracranial hypertension, when the usual therapy fails. With continuous perfusion, at high doses, of this agent, a state of lidocaine anesthesia can be induced which is more readily reversible than barbiturate anesthesia. A simultaneous anticonvulsant therapy is mandatory because of the well-known epileptogenicity of lidocaine. Closed cardiovascular monitoring is also needed to detect early signs of cardiotoxicity. Experimental works point to the effectiveness of i.v. lidocaine to prevent ischemic lesions secondary to a cerebral artery occlusion. This protective effect may result from some properties exhibited by lidocaine and not by thiopental: stabilisation of transmembrane ionic fluxes, inhibition of leucocytes intravascular sticking and tissular migration. So, i.v. lidocaine seems help to preserve or improve cerebral perfusion pressure and in cases when the latter decrease below the critical threshold, to protect against cerebral ischemia.
This paper studies the causes of hyperthermias occurring after a subarachnoid hemorrhage by ruptured aneurysm in 54 patients, totalizing 66 febrils episodes. Only 29 episodes bacteriologically proved infections. The profile of thermic curve, the hemodynamical profile, and clinical examination are not convincing. The most convincing elements for the diagnosis of infection are the increasing number of the leucocytes counts, the increasing curve of CRP, and simultaneous decreasing curve of C4. The evolution of these parameters permit to follow the efficiency of antibiotics.
From two cases of patients presenting a cerebral aneurysm associated with a dysplasia of elastic tissue, one a Marfan's syndrome, the other an anetoderma, this paper relate the post-operative, essentially cardio-vascularly and pulmonary complexities and define the elements of the pre-operative check-up.
In 34 patients admitted in Neurological Intensive Care Unit, for a cerebral hematoma by ruptured arterio-venous malformation, are present in 26 patients, on the first day. In many cases, the APTT is increased and this can be respected. These disorders do not seem to modify the incidence of delayed hemorrhage, except for the severe perturbances, related to a DIC or an hepatic deficiency. In these cases, the delayed hemorrhage must be prevented by transfusions of platelets and/or freeze fresh plasma.
This observation relates a case of spinal arachnoiditis with paraplegia, for a 56 year old patient hospitalized for a S.A.H. by a ruptured aneurysm of the P.I.C.A. This patient present some complications, requiring a prolonged ventilatory support with a tracheostomy, a ventricular shunt for hydrocephalus. The treatment is only surgical, and the corticosteroids delay the evolution, but without successful outcome.
The outcome of 35 patients in deep coma (GSS less than 7) due to an intracerebral hematoma following ruptured arteriovenous malformation (AVM) and admitted to a neurosurgical intensive care unit is reviewed. Eighty percent of these patients had a cerebral AVM and 20% had an AVM in the posterior fossa. All had a medical treatment of increase intracranial pressure (ICP). Twenty-four patients or 68.6% had an early surgical treatment or some days further and 13 had a good outcome, six had a persistent coma or a residual neurological deficit and five died. Four patients or 11.4% had an endovascular embolisation therapy and three had no satisfactory results and one died; all had a new intracranial hemorrhage with hematoma. Seven patients were not treated: four died before 48 hours of hospitalisation, one is in persistent coma and two are waiting an endovascular embolisation, alive but with a neurological deficit. The results suggest that neurosurgical treatment are a safe and effective means for treatment of these AVM with compressive intracranial hematoma.