Measurement of progressive cerebral ventriculomegaly in infants after grades III and IV intraventricular hemorrhages

To develop guidelines that might help predict prospectively which infants with severe intraventricular hemorrhage (IVH) would require intervention, we obtained serial cranial sonograms to measure the rate of growth of cerebral ventricular volumes in 48 preterm infants with and without IVH. The infants were divided into three groups: (1) those with no IVH (22 infants), (2) those with IVH with acute ventricular dilation (13 infants), and (3) those with IVH with progressive ventricular dilation requiring intervention (13 infants). The decision to intervene because of progressive ventricular dilation was based on clinical criteria and the subjective assessment of increasing ventricular size on weekly cranial sonograms. The rate of cerebral ventricular volume growth in infants with IVH who needed intervention was greater (4.2 +/- 3.3 ml/day) than that in infants without IVH (0.0 +/- 0.1 ml/day; p less than 0.001) and in infants with IVH and acute ventricular dilation (0.0 +/- 0.2 ml/day; p less than 0.001). Using these data, we generated guidelines for predicting prospectively which infants with IVH and ventricular dilation will need intervention for posthemorrhagic hydrocephalus. The guidelines were then confirmed prospectively in 10 infants.     

Measurement of the growth of the lateral ventricles in preterm infants with real-time ultrasound.

Real-time ultrasound was used to make exact measurements from the lateral wall of the body of the lateral ventricle to the falx (the ventricular index) in 273 infants of varying gestational ages. The measurement performed in an axial plane through the temporoparietal bone correlated closely with an actual measurement made in coronal plane in 50 infants. A cross-sectional centile chart was drawn up of the normal range for this measurement from 27 to 42 weeks'' postmenstrual age. A further chart showing the rate of change of the ventricular index allowed growth of the ventricles to be assessed in a longitudinal manner. Use of these charts permits early detection of hydrocephalus or dilated ventricles secondary to cerebral atrophy.     

Reference ranges for the linear dimensions of the intracranial ventricles in preterm neonates

AIMS: To establish normal ranges, in preterm infants < 33 weeks' gestation, for measurements of the lateral, third, and fourth ventricles and to assess intra-observer and inter-observer reliability. To assess the effect of head position during scanning on lateral ventricle size. To determine whether sex influences ventricle size. METHODS: A prospective study involving infants < 33 weeks' gestational age (GA) at birth. Cranial ultrasound scans were done during the first 3 days of life. Linear dimensions of the anterior horn width and thalamo-occipital distance of the lateral ventricles, the width of the third ventricle, and the width and length of the fourth ventricle were measured. Measurements were plotted against GA and reference ranges produced. All measurements were tested for intra-observer and inter-observer reliability. Head position and sex differences were studied. RESULTS: 120 infants with known GA (23(+1) to 32(+6) weeks) had their intracranial ventricles measured. Reference ranges obtained were-anterior horn width: 0-2.9 mm; thalamo-occipital distance: 8.7-24.7 mm; third ventricle width: 0-2.6 mm; fourth ventricle width: 3.3-7.4 mm; fourth ventricle length: 2.6-6.9 mm. Dependent and non-dependent lateral ventricles did not differ significantly in size. There was no clinically significant difference in ventricular size between sexes. CONCLUSIONS: Reference ranges for the measurement of the intracranial ventricles in preterm infants from 23 to 33 weeks' GA are provided and can be used in the diagnosis and assessment of ventricular enlargement in preterm infants. All measurements have good intra-observer and inter-observer reliability. Head position at the time of scanning does not influence the asymmetry of the lateral ventricular measurements. The infant's sex does not influence ventricular size.     

Serial lumbar punctures for at least temporary amelioration of neonatal posthemorrhagic hydrocephalus

Serial lumbar punctures for the management of neonatal posthemorrhagic hydrocephalus without intracranial hypertension were evaluated in 16 infants. Cranial ultrasonography to evaluate ventricular size and the Ladd monitor at the anterior fontanel to measure intracranial pressure were utilized immediately before and after lumbar puncture. In 12 patients, a decrease in ventricular size and in anterior fontanel pressure could be effected with each lumbar puncture. In these infants, cessation of progression of the hydrocephalus and intermittent decreases in ventricular size were accomplished. In four patients, lumbar punctures were not successful in decreasing ventricular size or lowering intracranial pressure. Two criteria could be defined to determine whether lumbar puncture could provide at least temporary benefit for the treatment of posthemorrhagic hydrocephalus. The first of these is to establish the presence of communication between lateral ventricles and lumbar subarachnoid space by effecting a decrease in ventricular size and a decrease in intracranial pressure by removal of CSF. The second criterion is to ascertain a critical volume of CSF (usually relatively large) that must be removed in order to effect the above changes. Cranial ultrasonography and measurement of intracranial pressure by application of the Ladd monitor to the anterior fontanel are extremely valuable in the evaluation of lumbar punctures in the management of posthemorrhagic hydrocephalus.     

Head size,brain growth,and lateral ventricles in very low birthweight infants.

Ninety eight newborn infants weighing less than 1500 g at birth and with gestational ages from 26 to 32 weeks were followed prospectively. They were grouped according to real time ultrasound scans in the neonatal period: infants in group A (n = 20) had periventricular haemorrhage (PVH) and normal ventricles; infants in group B (n = 26) had PVH and dilated ventricles (none with clinical hydrocephalus); and infants in group C, who formed the control group (n = 52), had no PVH and normal ventricles. At outpatient follow up a static image ultrasound scanner was used to measure the width of the lateral ventricles and brain hemispheres. The three groups of infants showed similar growth in occipitofrontal circumference, biparietal diameter, and brain hemispheres irrespective of a history of PVH or ventricular dilatation. The relation of ventricle size to biparietal diameter was similar in those infants in groups A (PVH alone) and C (controls) who had a good outcome. About a third (n = 8) of the infants in group B had persistent ventricular dilatation in relation to biparietal diameter and a poor outcome associated with developmental delay and cerebral palsy. By contrast, the remaining two thirds (n = 18) of the infants in group B who later had smaller ventricles in relation to biparietal diameter showed fewer neurodevelopmental sequelae. It is suggested that persistent ventricular dilatation in relation to biparietal diameter at follow up carries a bad prognosis, which might be due to brain atrophy.     

Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis

Symptomatic cerebral edema occurs in approximately 1% of children with diabetic ketoacidosis (DKA). However, asymptomatic or subclinical cerebral edema is thought to occur more frequently. Some small studies have found narrowing of the cerebral ventricles indicating cerebral edema in most or all children with DKA, but other studies have not detected narrowing in ventricle size. In this study, we measured the intercaudate width of the frontal horns of the lateral ventricles using magnetic resonance imaging (MRI) in children with DKA during treatment and after recovery from the DKA episode. We determined the frequency of ventricular narrowing and compared clinical and biochemical data for children with and without ventricular narrowing. Forty-one children completed the study protocol. The lateral ventricles were significantly smaller during DKA treatment (mean width, 9.3 +/- 0.3 vs. 10.2 +/- 0.3 mm after recovery from DKA, p < 0.001). Children with ventricular narrowing during DKA treatment (22 children, 54%) were more likely to have mental status abnormalities than those without narrowing [12/22 vs. 4/19 with Glasgow Coma Scale (GCS) scores below 15 during therapy, p = 0.03]. Multiple logistic regression analysis revealed that a lower initial PCO2 level was significantly associated with ventricular narrowing [odds ratio (OR) = 0.88, 95% confidence interval (95% CI) = 0.78-0.99, p = 0.047). No other variables analyzed were associated with ventricular narrowing in the multivariate analysis. We conclude that narrowing of the lateral ventricles is evident in just over half of children being treated for DKA. Although children with ventricular narrowing did not exhibit neurological abnormalities sufficient for a diagnosis of 'symptomatic cerebral edema', mild mental status abnormalities occurred frequently, suggesting that clinical evidence of cerebral edema in children with DKA may be more common than previously reported.     

Difference between left and right lateral ventricular sizes in neonates

The objective of this study is to determine the causes of asymmetry of the lateral ventricles in neonates. We also studied the effect of head position and the relationship of body weight at birth in regard to lateral ventricular size. Eligible for inclusion in this study were 60 neonatal infants whose gestational age was 33.1+/-3.5 weeks and whose birth weight was 1793+/-613 g. Ultrasonographic examinations were performed at the first and the second weeks after birth. In parasagittal and coronal scans through the posterior horn of the lateral ventricle, the lateral ventricle was traced and its area was measured. We found no significant variation of ventricular size in relation to body weight at birth. The left ventricular size was larger than the right one. The difference of the left and right ventricular sizes was partially effected by head position. The ratio of left to right lateral ventricular sizes showed a very wide distribution. We considered that ventricular asymmetry is not pathological, but due to individual differences.     

Progressive posthämorrhagische Ventrikelerweiterung des Frühgeborenen Inzidenz, Prognose und Therapie

Background. 35% of preterm infants with intraventricular hemorrhage develop ventricular dilatation. The posthemorrhagic ventricular dilatation can persist, be transient or be progressive. Finally 1–2% of all very low birthweight (VLBW <1500 g) infants require shunt placement for the treatment of the posthemorrhagic hydrocephalus. Outcome. The neurodevelopmental outcome is extremely poor in children surviving progressive posthemorrhagic ventricular dilatation. Therapy. There are no uniform guidelines for the treatment of preterm infants with progressive posthemorrhagic ventricular dilatation. Randomised multicenter trials demonstrated, that inhibition of cerebrospinal fluid production with acetazolamide and furosemide or early cerebrospinal fluid tapping did not reduce the need for shunt placement and may worsen the outcome or can be associated with adverse side-effects. Preterm infants with posthemorrhagic ventricular dilatation should be treated by standard therapy with uniform guidelines for cerebrospinal fluid tapping and shunt placement.     

Ventricular dilation following periventricular-intraventricular hemorrhage: outcome at age 1 year

Ventricular dilation following periventricular-intraventricular hemorrhage can be managed without ventriculoperitoneal shunting in most cases. Twenty-six patients who had periventricular-intraventricular hemorrhage with subsequent ventricular dilation were examined at 1 year of age for neurodevelopmental outcome and hydrocephalus. As previously reported, ventricular dilation may be divided into two groups: ventriculomegaly and posthemorrhagic hydrocephalus. Fourteen patients with ventriculomegaly were followed up with serial ultrasound observations only, and 12 patients with posthemorrhagic hydrocephalus had temporary drainage of ventricular fluid. Only three patients with posthemorrhagic hydrocephalus required ventriculoperitoneal shunting in the neonatal period. Neurodevelopmental abnormalities were found in eight infants who had posthemorrhagic hydrocephalus and two who had ventriculomegaly. Six of these infants had intraparenchymal injury demonstrated by ultrasound, five as a result of the original hemorrhage and 1 by infection. A single infant with posthemorrhagic hydrocephalus, discharged from the hospital with stable ventricular size, developed hydrocephalus and neurodevelopmental delay after the neonatal period. This reversed with ventriculoperitoneal shunting at 1 year of age. It is suggested that even in patients developing ventricular dilation following periventricular-intraventricular hemorrhage, it is the primary intraparenchymal injury that is responsible for subsequent morbidity. Thus, provided serial reevaluations are possible, an expectant management of ventricular dilation is justified.     

Transforming growth factor-beta1: a possible signal molecule for posthemorrhagic hydrocephalus?

Posthemorrhagic hydrocephalus remains a complication of preterm birth for which we lack a clear understanding and a curative therapy. Transforming growth factor beta (TGF-beta) is a cytokine that upregulates the production by fibroblasts of extracellular matrix proteins. We hypothesized that TGF-beta might be released into cerebrospinal fluid (CSF) after intraventricular hemorrhage and play a role in posthemorrhagic hydrocephalus. Total TGF-beta1 and TGF-beta2 were measured by immunoassay in CSF samples from 12 normal preterm infants, nine preterm infants with transient posthemorrhagic ventricular dilation, and 10 infants who subsequently developed permanent hydrocephalus. Five infants received intraventricular tissue plasminogen activator, and two infants were treated by drainage irrigation and fibrinolytic therapy. Median TGF-beta1 in normal CSF was 0.495 ng/mL. In infants with transient posthemorrhagic ventricular dilation, median initial CSF TGF-beta1 was 2.1 ng/mL. Infants who subsequently had permanent hydrocephalus had median initial CSF TGF-beta1, 9.7 ng/mL (differences between groups p < 0.01). Intraventricular recombinant tissue plasminogen activator was followed by a rise in CSF TGF-beta1 (p = 0.0007). Drainage irrigation and fibrinolytic therapy was followed by a fall in CSF TGF-beta1. TGF-beta2 was detected in CSF and showed similar trends, but the CSF concentration of TGF-beta1 was more than 20 times higher. These findings support the hypothesis that TGF-beta1 is released into CSF after intraventricular hemorrhage and may play an important part in hydrocephalus. The results help to explain the failure of intraventricular fibrinolytic therapy.     

Cranial ultrasound and clinical studies in preterm infants

Serial ultrasound imaging of the brain was used to determine the ventricular index (VI), and the ratio (VR) of the VI to the cranial hemidiameter during the nursery course and first year post-term in preterm infants of less than 33 weeks gestation. Twenty-nine of the infant survivors with no intracranial hemorrhage or major medical complication during their nursery course composed group 1. Twenty-two survivors with intracranial hemorrhage unassociated with early ventricular dilation composed group 2. Group 3 was comprised of 10 other survivors who had neonatal intraventricular hemorrhage with early ventriculomegaly; all 10 infants had at least one major medical complication during their neonatal course. In groups 1 and 2 the VR decreased and the VI increased significantly with age post-conception. Infants in group 3, compared with those in groups 1 or 2, had decreased occipitofrontal growth during the early postnatal period and increased VR and VI during the neonatal period and first year post-term. These results suggest that the ventriculomegaly associated with neonatal intracranial hemorrhage cannot be explained by posthemorrhagic hydrocephalus alone and may also be related to cerebral atrophy or decreased brain growth or both. Neurodevelopmental assessments at 20 to 30 months of age disclosed significantly lower Bayley Motor Development scores in group 3 compared with groups 1 or 2. Four infants in group 3, but none in groups 1 or 2, had cerebral palsy. The neurodevelopmental deficits in group 3 infants may reflect the complex pathogenesis of the ventriculomegaly as well as the effects of the intraventricular hemorrhage and posthemorrhagic hydrocephalus.     

Fetal lamb ventricles respond differently to filling and arterial pressures and to in utero ventilation

Right and left ventricular function were investigated in 12 fetal lambs (127-140 days gestation) instrumented with electromagnetic flow sensors on the ascending aorta and the main pulmonary artery, and with vascular catheters. Nine fetuses were equipped with a postductal aortic occluder and the trachea was cannulated in eight. Control arterial blood values were pH 7.36 +/- 0.02 (SD), PCO2 49.3 +/- 2.3 torr, PO2 18.4 +/- 1.7 torr, and hematocrit 37.3 +/- 4.4%. Biventricular function curves relating stroke volume to mean right and left atrial pressure were generated by rapid withdrawal and reinfusion of fetal blood. Both function curves were composed of steep ascending and plateau limbs that intersected at a breakpoint. Stroke volumes at the breakpoints were 0.94 +/- 0.19 ml.kg-1 and 0.63 +/- 0.15 ml.kg-1 for right and left ventricle, respectively (p less than 0.001). During postductal aortic occlusion, arterial pressure increased by 19.3 +/- 7.9 torr while right ventricular stroke volume decreased by approximately 48% and left ventricular stroke volume decreased by approximately 9%. In utero ventilation increased arterial pressure, heart rate, PO2, and oxygen content. Right atrial pressure increased from 3.9 +/- 1.3 to 5.8 +/- 2.9 torr (p less than 0.05); left atrial pressure from 3.5 +/- 1.5 to 10.0 +/- 4.4 torr (p less than 0.05). Aortic flow nearly doubled (112 +/- 29 to 211 +/- 35 ml.min-1.kg-1) (p less than 0.05), and the left ventricular function curve shifted upward. The right ventricular function curve was shifted downward during ventilation. We conclude that the fetal ventricles differ significantly in their outputs, response to changes in arterial pressure, and to the onset of in utero ventilation.     

Cerebral ultrasound diagnosis in brain abnormalities

Gray scale ultrasonography of the brain was performed in 93 infants with cerebral malformations. The most common malformation was the Chiari-malformation (56 children), characterized by the caudal displacement of the cerebellar vermis into the foramen magnum. The rest of the cerebellum, pons and medulla oblongata were displaced caudally and dysplastic. All children with Chiari-syndrome showed more or less severe hydrocephalus. The Dandy-Walker-malformation (3 children) was characterized by a huge retrocerebellar cyst communicating with the fourth ventricle. The cerebellar vermis was dysplastic. In alobar holoprosencephaly (2 children) a large singular midline ventricle could be shown. Both thalami and plexus chorioidei were fused in the midline. Absence of the falx cerebri, interhemispheric fissure, corpus callosum and septum pellucidum was characteristic for alobar holoprosencephaly. Stenosis of the Sylvian aqueduct (4 children) was characterized by enlarged lateral ventricles and third ventricle, whereas the fourth ventricle was normal in size. Porencephalic cysts (7 children) were spheric echofree lesions of various size, usually located symmetrically in both cerebral hemispheres. In hydranencephaly (4 children) both hemispheres were replaced by echofree space occupying bubbles. In 5 children with agenesis of the corpus callosum no corpus callosum could be demonstrated by sonography. Coronal sections displaced the typical bull's head shape, formed by the enlarged third ventricle and the side ventricles as well as randomly arrayed sulci around the lateral ventricles, which are pathognomonic for agenesis of the corpus callosum. Agenesis of the septum pellucidum (5 children) was characterized by fusion of the frontal horns of the lateral ventricles. One child with aneurysmatic malformation of the vein of Galen showed dilated sinus rectus and pulsations of a cyst, located behind the third ventricle. Pulsed doppler recording showed pulsatile arterial flow patterns within the cyst.     

The contractility and performance of the preterm left ventricle before and after early patent ductus arteriosus occlusion in surfactant-treated lambs

The influence of left-right ductal shunting on early hemodynamic responses, namely left ventricular performance, contractility, and systemic perfusion was evaluated in nine preterm lambs (120 days gestational age) treated with surfactant. Blood gases were maintained in the physiological range using mechanical ventilation; hemodynamic and blood flow measurements (radionuclide labeled microspheres) were obtained before and after occlusion of the patent ductus arteriosus with a catheter balloon. The mean left-right ductal shunt before occlusion (1.2 h postnatal age) was 59 +/- 11% SD. Left ventricular output was increased in all lambs with PDA (pre: 306 +/- 106 versus post: 155 +/- 31 ml/min/kg; p less than 0.001); effective systemic blood flow and organ blood flows did not change. The left ventricle end-diastolic volume was increased in all and decreased following ductal occlusion (pre: 2.0 +/- 0.4 versus post: 1.5 +/- 0.2 ml/kg; p less than 0.01). Cardiac rate, ejection fraction, and contractility (peak dP/dt) did not change. Right-left ductal shunting was not detected in six similarly treated lambs. Thus, during the 1st h of life the hemodynamic profile of preterm lambs with patent ductus arteriosus was characterized by large magnitude left-right shunt and a "high" cardiac output state sufficient to maintain unchanged systemic perfusion. The increased left ventricle output was accomplished by increasing end-diastolic volume (Frank-Starling mechanism), but left ventricle contractility remained unchanged. We speculate that the preterm left ventricle may be unable to sustain the high level of pump performance and contractility required to compensate for the ductal "steal" of systemic blood flow.     

Soluble Fas (CD95/Apo-1), soluble Fas ligand,and activated caspase 3 in the cerebrospinal fluid of infants with posthemorrhagic and nonhemorrhagic hydrocephalus

Hydrocephalus may result in loss of tissue associated with neuronal degeneration, axonal damage, and reactive gliosis. The soluble form of the anti-apoptotic regulator Fas (sFas) and the pro-apoptotic factors soluble FasL (sFasL) and activated caspase 3 were studied in the cerebrospinal fluid of infants with hydrocephalus. Fifteen preterm infants with posthemorrhagic hydrocephalus undergoing serial reservoir puncture and seven term or near-term infants with nonhemorrhagic hydrocephalus and shunt surgery were included in the study. Twenty-four age-matched patients with lumbar puncture for the exclusion of meningitis served as controls. Elevated levels of sFas were observed in infants with posthemorrhagic hydrocephalus [median (range), 131 ng/mL (51-279 ng/mL)] and in nonhemorrhagic hydrocephalus [127 ng/mL (35-165 ng/mL)]. sFas concentrations were highest in a subgroup of eight patients with posthemorrhagic hydrocephalus developing periventricular leukomalacia [164 ng/mL (76-227 ng/mL)]. In contrast, in 24 control infants, sFas was low, in 15 cases below detection limit (0.5 ng/mL) and in nine cases, 24 ng/mL (20-43 ng/mL). sFasL and activated caspase 3 did not differ from control infants in all groups of patients. Increased intrathecal release of sFas in the cerebrospinal fluid of infants with hydrocephalus may serve as an indicator of brain injury from progressive ventricular dilatation.     

Ventricular volume in infantile hydrocephalus and its relationship to intracranial pressure and cerebrospinal fluid clearance before and after treatment. A preliminary study

The present study examines ventricular volume before and after shunting in 16 infants with hydrocephalus and mixed aetiology and relates this parameter to rates of cerebrospinal fluid clearance, intracranial pressure and outcome. Following treatment all patients showed reduction in intracranial pressure and amelioration of the clinical manifestations of hydrocephalus. Nevertheless, 4 patients showed persistence of marked ventriculomegaly, 4 had moderate ventricular enlargement, while 8 showed small or normal ventricles. Although the series was small there appeared to be a clear correlation between persistent ventriculomegaly, poor cerebrospinal fluid clearance and poor outcome despite reduction in intracranial pressure. The question is raised as to whether pressure-determined cerebrospinal fluid drainage provides optimum treatment of hydrocephalus in infants given the particular physical characteristics pertaining to the non-rigid cranium.     

Cerebrovascular hemodynamics during and after recovery from acute asphyxia in the newborn dog

Cerebrovascular volume and transmural pressure loads accompanying acute increases in cerebral blood flow are implicated in the pathogenesis of periventricular-intraventricular hemorrhage in preterm infants. An acute increase in cerebral blood flow would be expected during acute recovery from asphyxia. Therefore, cerebrovascular hemodynamics, including flow (microspheres), were studied during and after acute recovery from asphyxia in seven newborn dogs in order to study the determinants of these volume and pressure loads. During the acute recovery phase, cerebral hemispheric blood flow was 69.6 +/- 10 ml/100 g/min (mean +/- SEM) representing a 250% increase from baseline values of 19.9 +/- 1.8 ml/100 g/min (p less than 0.005), while combined cerebellar-brainstem flow was 204.3 +/- 19.3 ml/100 g/min representing a 536% increase from baseline values of 32.0 +/- 1.5 ml/100 g/min (p less than 0.005). Blood flow to both areas had returned to baseline levels 20 min after the onset of recovery. Associated with this cerebral hyperemia was an acute increase in mean arterial pressure from 21.3 +/- 4.5 mm Hg at end asphyxia to 69.5 +/- 6.0 mm Hg at peak recovery (p less than 0.01), and parallel acute increases in sagittal sinus pressure (from 4.0 +/- 0.4 to 14.6 +/- 1.9 mm Hg, p less than 0.01) and cerebrospinal fluid pressure (from 3.8 +/- 0.4 to 14.3 +/- 1.9 mm Hg, p less than 0.01). Central venous pressure fell from 4.3 +/- 0.6 mm Hg at end asphyxia to 1.6 +/- 0.5 mm Hg, and thus is not a determinant of the elevation in sagittal sinus pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes of third ventricle diameter (TVD) mirror changes of the entire ventricular system after initial therapy and during follow-up in pediatric hydrocephalus

PurposeRegular measurement of ventricular size is important in children with hydrocephalus. After closure of the fontanelle this is currently addressed by repetitive cranial MRI or CT imaging, coming along with risks of anaesthesia or radiation. As the third ventricle is accessible via the temporal bone window using ultrasound, determination of its diameter might be an easy and radiation-free alternative to assess the ventricular system. An essential precondition is that changes of the third ventricle diameter (TVD) mirror changes of the whole ventricular system. This study compares changes of TVD with changes of ventricular indices before and after initial treatment of hydrocephalus and during the following evolution.MethodsMRT/CT images from 117 children with hydrocephalus were evaluated at time of diagnosis, after initial therapy and during follow-up with functional shunts. Measurements included axial TVD and three standard linear measures of the lateral ventricles (Evans Index - EI, fronto-occipital horn ratio - FOHR Index, and Cella Media Index - CMI). Furthermore, a correlation within subjects was calculated in 8 patients over the entire available follow-up.ResultsRelative changes of TVD were significantly correlated to relative changes of all ventricular indices (r = 0.48, r = 0.68 and r = 0.701 for EI, FOHR and CMI, respectively, p < 0.01). The correlation within subjects was outstanding for EI (r = 0.988), FOHR (r = 0.99) and CMI (r = 0.99).ConclusionTVD showed a significant correlation with all three linear indices at the time of diagnosis and during follow-up changes independently of age, aetiology and ventricular width. TVD and its changes are therefore a reliable surrogate of changes in ventricular size in pediatric hydrocephalus undergoing treatment.     

CSF removal in infantile posthemorrhagic hydrocephalus results in significant improvement in cerebral hemodynamics

Rational intervention in infants with posthemorrhagic hydrocephalus (PHH) would be facilitated greatly by bedside measure of impaired cerebral perfusion, as there is substantial evidence that impaired perfusion and oxidative metabolism contribute to irreversible brain injury in hydrocephalus. Near-infrared spectroscopy (NIRS) measures changes in the cerebral concentration of oxygenated and deoxygenated hemoglobin and oxidized cytochrome oxidase at the bedside of infants continuously and noninvasively. The total hemoglobin and the hemoglobin difference signal are derived from the sum and difference, respectively, of oxygenated and deoxygenated hemoglobin. Changes in total hemoglobin reflect changes in cerebral blood volume; our previous work has shown that changes in hemoglobin difference signal reflect changes in cerebral blood flow. We hypothesized that cerebrospinal fluid (CSF) removal in infants with PHH would result in significant increases in cerebral perfusion, cerebral blood volume, and oxidative metabolism, as measured by NIRS. Continuous NIRS recordings were performed during CSF removal on 16 infants with PHH. There was a statistically significant increase in oxygenated hemoglobin (p < 0.001), total hemoglobin (p = 0.001), and hemoglobin difference signal (p = 0.006), but not oxidized cytochrome oxidase, accompanying CSF removal. There was no significant correlation between either the volume of CSF removed (in milliliters per kilogram body weight) or the opening pressure and the change in any of the measured or calculated NIRS signals. These findings demonstrate the pronounced effect of CSF removal on cerebral perfusion in infants with PHH. NIRS may be a useful technique to detect impending cerebral ischemia in such infants and thereby provide a means to guide the rational management of PHH.     

Measurement of right ventricular volume in healthy term and preterm neonates

BACKGROUND: Pulmonary hypertension is associated with worse perinatal outcomes in infants with respiratory disorders. In such infants right ventricular dysfunction may result in poor pulmonary blood flow. OBJECTIVE: To evaluate the practicability and repeatability of echocardiographic measurements of right ventricular volume in healthy term and preterm neonates, and to follow changes in right ventricular volume over the first 2 days of life. METHODS: Serial echocardiographic examinations were performed on day 0, 1, and 2 on healthy term and preterm neonates. Two methods of estimating right ventricular volume were assessed: the ellipsoid approximation and Simpson's stacked discs methods. Systolic and diastolic volumes on days 1 and 2 were compared with baseline values on day 0. Term and preterm volumes were compared at the same time points. RESULTS: Thirty five infants were recruited, 18 term and 17 preterm. Right ventricular volumes were significantly lower on day 1 and day 2 than baseline in both term and preterm infants. Median (interquartile range) end systolic and diastolic volumes for term infants on days 0, 1, and 2 were 1.04 (0.88-1.44), 0.82 (0.70-1.03), 0.92 (0.72-0.97) ml/kg and 2.21 (2.10-2.75), 2.05 (1.81-2.38), 1.91 (1.81-2.13) ml/kg respectively. In preterm infants the values were 1.09 (0.91-1.16), 0.72 (0.54-0.91), 0.61 (0.54-0.76) ml/kg and 2.09 (1.71-2.25), 1.47 (1.23-1.98), 1.43 (1.22-1.78) ml/kg respectively. CONCLUSION: Right ventricular volume decreases over the first 2 days of life in healthy term and preterm infants.