Silent cerebral infarction in hemodialysis patients: possible predictors for vascular events

We designed this study on hemodialysis [HD] patients to estimate the prevalence of silent brain infarction [SBI]; to evaluate the cardiovascular risk factors for SCI; and to investigate whether or not SCI is associated with clinical vascular events. Fifty HD patients who had no past history of stroke or TIA were included in this prospective study. We followed these patients for two years to record any vascular events related to cardiovascular or cerebrovacsular diseases. All patients underwent CT or MRI on the brain to define any silent brain infarcts. We investigated the prognostic role of SCI in cerebral, cardiac and vascular events by using Cox proportional hazards analysis. SCI was detected in 16 patients out of 50 HD patients with a percentage of 32%. During follow up period, vascular events were detected in ten patients after two years of follow up; six cerebral events; three cardiac events; and one death. The HD patients group with SCI had none significantly higher cerebral and cardiac morbidity than the group without SCI. Patients with SCI were significantly older than those without SCI and had significantly longer duration of HD. Furthermore, HD patients with SCI had significantly higher systolic and diastolic blood pressure than those without SCI. We could not find a difference between HD patients with SCI and those without SCI as regards other cardiovascular risk factor except for ischemic heart disease [IHD]. Using univariate analysis, we found that age, duration of HD, IHD and silent brain infarction were predictors of vascular events, whereas, duration of HD and SCI were predictors of cerebral events. By multivariate analysis, we found that SCI was a powerful independent predictor of cerebral and vascular events. We concluded that the presence of SCI is an independent risk factor for vascular events in HD patients

Recurrent bacterial meningitis in children role of imaging

Recurrent bacterial meningitis may be the consequence of immune deficiency or result from anatomic abnormalities which provide portals of entry of infection into the central nervous system. Bacterial migration along congenital or acquired pathways from the skull or spinal dural defects gain entrance into the CNS and should be taken into consideration when children face recurrent bacterial meningitis. Assess the role of imaging in children with recurrent bacterial meningitis 10 children with Recurrent bacterial meningitis were included in this study. They were 8 males and 2 females. Their age ranged from 2-16 years. All patients were subjected to CT scan for brain and skull base. CT metrizamide was done in 7 cases, cranial MRI in 3 cases and spinal MRI in one case. Cranial dural defects were found in 9 cases. These defects were traumatic [3 cases], congenital [4], chronic increased intracranial pressure [1] and in 1 case we were not able to identify the exact nature either congenital or acquired. One child has spinal dural defect due to congenital dermal sinus of the lumbar spine. Among the helical CT scanners used in this study [single, 4 and 64 slices], the 64-slice scanner was very sensitive to small cranial dural defects while CF metrizamide was sensitive and specific for defect localization. Recurrent bacterial meningitis should prompt a search for an underlying cranial or spinal anatomic detects especially in the absence of immunodeficiency conditions

Urinary excretion of glycosaminoglycans and ultrasound urinary bladder wall thickness in children with refractory primary nocturnal enuresis

This study was undertaken to determine variations in the amount of glycosaminoglycans [GAGs] excreted by patients with refractory primary nocturnal enuresis [RPNE], and assessment of associated bladder dysfunction with the use of a special ultrasound [US] protocol, as prediction of pathophysiology of refractory primary nocturnal enuresis and associated bladder dysfunction. The study included 30 children with [RPNE] with mean age 7.33 +/- 2.23 and 30 healthy age matched control children with mean age 8.9 +/- 1.68 years. All patients more than 5 years old were treated for primary nocturnal enuresis [PNE] with behavioral therapy and desmopressin for at least 6 months with no response. The studied groups were subjected to the following complete medical history, physical examination, urine analysis and their urinary GAGs excretion was assessed over 24 h using the sodium tetraboratecarbazole method. Plain KUB, and abdominal ultrasound using special protocol was designed for the evaluation of bladder parameters using bladder volume and wall thickness index [BVWI%], and expected percentage bladder volume index for kidney volume. Patients with refractory primary nocturnal enuresis had higher mean values of urinary GAGs excretion than age-matched controls. Also they had low bladder capacity and thick bladder wall more than age-matched. The mean urinary GAGs contents were 38.9, and 27.5 mg/g creatinine in patients with RPNE and controls respectively; [P<0.001]. Comparing the BVWI in normal and enuretic children in correlation with functional bladder capacities we found that patients with low capacity thick bladder wall also have high GAGs excretion. Measuring urinary GAGs excretion and Ultrasound bladder wall thickness can be used as predictive pathophysiological clues, for underlying bladder dysfunction, which has an important role in the pathophysiology of enuresis especially in refractory cases. Also they can minimizing the need for invasive urodynamic study in children with RPNE for assessing bladder wall dysfunction