Regional lidocaine infusion reduces postischemic spinal cord injury in rabbits.

Paraplegia secondary to spinal cord ischemia is a devastating complication in operations on the descending and thoracoabdominal aorta. We hypothesized that the tolerance of the spinal cord to an ischemic insult could be improved by means of regional administration of lidocaine. Thirty-one New Zealand white rabbits were anesthetized and spinal cord ischemia was induced by the placement of clamps both below the left renal vein and above the aortic bifurcation. The animals were divided into 5 groups. Aortic occlusion time was 20 minutes in Group 1 and 30 minutes in all other groups. Groups 1 and 2 functioned as controls. Lidocaine (Group 5) or normal saline solution (Group 3) was infused into the isolated aortic segment after cross-clamping. Group 4 animals received 20% mannitol regionally, before and after reperfusion. Postoperatively, rabbits were classified as either neurologically normal or injured (paralyzed or paretic). Among controls, 20 minutes of aortic occlusion did not produce any neurologic deficit (Group 1: 0/4 injured), while 30 minutes of occlusion resulted in more consistent injury (Group 2: 6/8 injured). Animals that received normal saline (Group 3) or mannitol (Group 4) regionally showed 80% neurologic injury (4/5). Animals treated with the regional lidocaine infusion (Group 5) showed much better neurologic outcomes (7/9 normal: 78%). This superiority of Group 5 over Groups 2, 3, and 4 was significant (P <0.02). We conclude that regional administration of lidocaine reduced neurologic injury secondary to spinal cord ischemia and reperfusion after aortic occlusion in the rabbit model.     

Beneficial effects of iloprost during experimentally induced hemorrhagic shock

BACKGROUND: The aim of the study was to evaluate the efficacy of iloprost on myocardial insufficiency associated with hypovolemic shock in dogs. We designed the study as a controlled randomized study. METHODS: Sixteen mixed-breed dogs were included into the study and divided into two equal groups as the control and iloprost groups. Mean arterial pressure was reduced to 45 mmHg by withdrawing the arterial blood into citrated bags. The control group did not receive any drug but the other group received iloprost at a rate of 20 ng/kg/min by an infusion pump. Iloprost infusion was started 30 min after the blood pressure was reduced to 45 mmHg. All measurements were made before removal of blood, 45 min after exsanguination and at 1 hour intervals for 3 hours. Left ventricular stroke work index was measured 72 hours after the study. The hemodynamic and biochemical parameters and blood gas analysis were obtained. RESULTS: After hemorrhage, cardiac index (CI) decreased significantly from 132 +/- 14 to 51 +/- 8 ml/kg/min in the control group and from 128 +/- 11 ml/kg/min to 47 +/- 13 ml/kg/min in the iloprost group, respectively but at the end of the third hour it was 81 +/- 8 ml/kg/min in the control group and 105 +/- 6 ml/kg/min in the iloprost group (p < 0.05). Tumor necrosis factor-alpha (TNF alpha) was 41 +/- 8 pg/ml in the control group and 18 +/- 6 in the iloprost group 3 hours after bleeding (p < 0.05). Tumor necrosis factor-alpha concentration was significantly higher in the control group than in the iloprost group. There was no significant difference in pH between the groups but actual bicarbonate concentrations were different between the groups (p < 0.05). At the end of the third hour total body oxygen consumption was 105 +/- 11 ml/min in the control group and 132 +/- 12 ml/min in the iloprost group (p < 0.05). Oxygen delivery 3 hours after hemorrhage was 201 +/- 19 ml/min in the control group and 252 +/- 24 ml/min in the iloprost group (p > 0.05). Left ventricular stroke work index was higher in the iloprost group (p < 0.05). CONCLUSIONS: Hemorrhagic shock causes tumor necrosis factor-alpha release which may lead to multiple organ failure. Organ dysfunction still persists even after the appropriate treatment. Iloprost attenuates the release of tumor necrosis factor-alpha which may improve the adverse effects of hemorrhagic shock.     

Progressive facial hemiatrophy (Parry-Romberg syndrome)

A 48-year-old white woman presented with a 2-year history of progressive facial hemiatrophy involving the right side of the chin and tongue, associated with mastigatory spasm. Neurological examination showed no abnormalities. Computed tomography and magnetic resonance imaging of the brain and electrophysiological investigations were normal. Histopathological examination of a skin biopsy specimen from the chin revealed atrophy of the subcutaneous fat with homogenization of dermal collagen fibres. Phenytoin 100 mg t.d.s. relieved the mastigatory spasm.     

Acute orbital effects of retrobulbar injection on optic nerve head topography

AIM: To assess the effects of acute orbital volume changes after retrobulbar injection on optic nerve head topography. METHODS: The study population consisted of 95 patients with type 2 diabetes mellitus with clinically significant macular oedema who required focal pattern laser photocoagulation therapy in one eye. Before each laser treatment, 49 patients required a retrobulbar injection (approximately 7 ml of a mix of lidocaine 2% with epinephrine and bupivacaine 0.75% in equal volumes) to provide ocular akinesia. Both eyes of all patients underwent optic nerve head topographic analysis once before laser treatment (within 30 minutes), and repeated within 1 hour, 1 day, 1 week, 2 weeks, and 4 weeks after treatment, respectively. Topographic analyses were performed using a confocal scanning laser ophthalmoscope, HRT-II. The disc area, topography standard deviation, and a total of 12 topographic parameters were calculated by HRT-II. RESULTS: The mean age of the patients was 37.9 (SD 3.2) years. The mean disc area of the subjects was 2.12 (0.44) mm(2). Fellow eyes which were not treated with laser, and those treated eyes which did not receive retrobulbar injection before therapy were found not to reveal significant changes in disc topography in any of the examinations (all p values >0.05). In the topographic examinations in the first hour, first day, and first week, laser treated eyes which underwent retrobulbar injection demonstrated significant increase in the disc area, rim area, rim volume, rim area/disc area, and cup shape measure parameters while optic cup parameters significantly decreased (all p values <0.05). In the second week examinations, they did not show significant difference in disc area measurements (p>0.05). By the fourth week, all of the optic nerve head topographic variables were not significantly different from the pre-injection values (all p values >0.05). Colour stereoscopic photographs did not reveal any differences in optic disc appearance. CONCLUSION: Acute orbital volume change following retrobulbar injection may cause significant topographic evidence of optic disc oedema lasting approximately 1 week. Significant changes in optic rim and cup area may last for 2 weeks after injection, with all topographic changes returning to baseline by 1 month after injection. The present findings could be a model to reflect the pathological processes that occur in cases of acute orbital volume changes such as retrobulbar haemorrhage.     

Cost of renal replacement therapy in Turkey

BACKGROUND AND RESULTS: By the end 2000, 22224 patients were on renal replacement therapy (RRT) in Turkey. We investigated the cost of RRT in three medical faculties and one private dialysis centre. Yearly expenses were US dollars 22759 for haemodialysis (HD), US dollars 22350 for continuous ambulatory peritoneal dialysis (CAPD), and US dollars 23393 and US dollars 10028, respectively, for the first and second years of transplantation (Tx). In the first year, renal Tx was significantly more expensive than CAPD. However, after the first year of renal transplantation, Tx became significantly more economical than both CAPD and HD. The sum of all yearly RRT expenses for the country was US dollars 488958709, which corresponds to nearly 5.5% of Turkey's total health expenditure. CONCLUSION: Measures such as early construction of vascular access, promoting home dialysis and the reuse of the dialysers, strict control of the use of some expensive drugs like erythropoietin and active vitamin D, and also increasing the number of transplantations, especially if pre-emptive transplantation is possible, should be taken into account in order to reduce these expenses.     

Parkinson disease neuropathology: later-developing dementia and loss of the levodopa response.

OBJECTIVE: To investigate the neuropathologic substrate for dementia occurring late in Parkinson disease (PD). DESIGN: We identified 13 patients with a clinical diagnosis of PD who experienced dementia at least 4 years after parkinsonism onset (mean, 10.5 years) and subsequently underwent postmortem examination. Despite levodopa therapy, 9 patients later became severely impaired and nonambulatory, requiring total or near-total care; this included 4 patients treated with 1200 mg/d or more of levodopa (with carbidopa), which was consistent with loss of the levodopa response. These 13 patients were compared with 9 patients clinically diagnosed as having PD, but without dementia, who had undergone autopsies. RESULTS: Twelve of 13 PD patients with dementia had findings of diffuse or transitional Lewy body disease as the primary pathologic substrate for dementia; 1 had progressive supranuclear palsy. This pathology also apparently accounted for the levodopa refractory state. Among the 12 PD patients with dementia, mean and median Lewy body counts were increased nearly 10-fold in neocortex and limbic areas compared with PD patients without dementia (P< or =.002). Alzheimer pathology was modest. Only one patient met the criteria defined by the National Institute on Aging and the Reagan Institute Working Group on the Diagnostic Criteria for the Neuropathologic Assessment of Alzheimer's Disease for "intermediate probability of Alzheimer's disease." There were, however, significant correlations between neocortical Lewy body counts and senile plaques as well as neurofibrillary tangles. Senile plaque counts did not significantly correlate with tangle counts in any of the analyzed nuclei. Arteriolar disease may have contributed to the clinical picture in 2 patients. CONCLUSIONS: Diffuse or transitional Lewy body disease is the primary pathologic substrate for dementia developing later in PD. This same pathologic substrate seemed to account for end-stage, levodopa refractory parkinsonism. The occurrence of Alzheimer pathology was modest, but was highly correlated with Lewy body pathology, suggesting common origins or one triggering the other.