Poor Long-term Neurological Outcome Research Articles

Plasma proenkephalin A 119–159 and dipeptidyl peptidase 3 on admission after cardiac arrest help predict long-term neurological outcome

BackgroundA large proportion of adult survivors of cardiac arrest have a poor neurological outcome. Guidelines recommend multimodal neuro-prognostication no earlier than 72–96 h after cardiac arrest. There is great interest in earlier prognostic markers, including very early markers at admission. The novel blood biomarkers proenkephalin A 119–159 (penKid), bioactive adrenomedullin (bio-ADM) and circulating dipeptidyl peptidase 3 (cDPP3) have not been previously investigated for the early prognosis of cardiac arrest survivors. MethodsThis multicentre observational study included adult survivors of cardiac arrest admitted to intensive care at four Swedish intensive care units (ICUs) during 2016. Blood samples were collected at ICU admission and batch analysed. The association between admission plasma penKid, bio-ADM and cDPP3 and poor long-term neurological outcome, according to the Cerebral Performance Category (CPC) scale, was assessed by binary logistic regression. Their prognostic performance was assessed using the area under the receiver operating characteristic curve (AUC). ResultsA total of 190 patients were included, of which 136 patients had suffered out-of-hospital and 54 patients in-hospital cardiac arrest. Poor long-term neurological outcome was associated with elevated admission plasma concentrations of penKid and cDPP3, but not with bio-ADM. The association for penKid, but not for cDPP3, remained after adjusting for clinical cardiac arrest variables with prognostic value (time to return of spontaneous circulation (ROSC), initial rhythm, admission Glasgow coma scale (GCS) motor score and absence of pupillary reflexes). The prognostic performance of above mentioned clinical cardiac arrest variables alone was very good with an AUC of 0.90 (95% confidence interval, CI, 0.86–0.95), but improved further with the addition of penKid resulting in an AUC of 0.93 (95% CI 0.89−0.97, p < 0.026). Plasma penKid and cDPP3 alone provided moderate long-term prognostic information with AUCs of 0.70 and 0.71, respectively. ConclusionAfter cardiac arrest, admission plasma levels of penKid and cDPP3, but not bio-ADM, predicted long-term neurological outcome. When added to clinical cardiac arrest variables, penKid further improved prognostic performance.

Sequence Variation in the DDAH1 Gene Predisposes for Delayed Cerebral Ischemia in Subarachnoidal Hemorrhage.

Delayed cerebral ischemia (DCI) often causes poor long-term neurological outcome after subarachnoidal hemorrhage (SAH). Asymmetric dimethylarginine (ADMA) inhibits nitric oxide synthase (NOS) and is associated with DCI after SAH. We studied single nucleotide polymorphisms (SNPs) in the NOS3, DDAH1, DDAH2, PRMT1, and AGXT2 genes that are part of the L-arginine–ADMA–NO pathway, and their association with DCI. We measured L-arginine, ADMA and symmetric dimethylarginine (SDMA) in plasma and cerebrospinal fluid (CSF) of 51 SAH patients at admission; follow-up was until 30 days post-discharge. The primary outcome was the incidence of DCI, defined as new infarctions on cranial computed tomography, which occurred in 18 of 51 patients. Clinical scores did not significantly differ in patients with or without DCI. However, DCI patients had higher plasma ADMA and SDMA levels and higher CSF SDMA levels at admission. DDAH1 SNPs were associated with plasma ADMA, whilst AGXT2 SNPs were associated with plasma SDMA. Carriers of the minor allele of DDAH1 rs233112 had a significantly increased relative risk of DCI (Relative Risk = 2.61 (1.25–5.43), p = 0.002). We conclude that the DDAH1 gene is associated with ADMA concentration and the incidence of DCI in SAH patients, suggesting a pathophysiological link between gene, biomarker, and clinical outcome in patients with SAH.

Abstract 13682: Single Nucleotide Polymorphisms in the Ddah1 Gene Are Associated With Delayed Cerebral Ischemia in Patients With Subarachnoid Hemorrhage

Introduction: Delayed cerebral ischemia (DCI) is a major cause of lethality and poor long-term neurological outcome in patients with subarachnoid hemorrhage (SAH). Asymmetric (ADMA) and symmetric dimethylarginine (SDMA) are regulators of vascular NO synthesis from L-arginine. We previously reported that elevated concentrations of both, ADMA and SDMA at ICU admission are associated with the incidence of DCI during follow-up. Dimethylarginines (DMAs) are synthesized by PRMT enzymes; ADMA is metabolized by DDAH1 and DDAH2, whilst SDMA is metabolized by AGXT2. Hypothesis: We hypothesized that common genetic variants in genes encoding the core enzymes of DMA metabolism may predispose individuals for the development of DCI after SAH. Methods: We measured L-arginine, ADMA and SDMA in plasma and cerebrospinal fluid (CSF) of 51 SAH patients at ICU admission and followed them for clinical status and neurological outcome until 30 days post-discharge. Single nucleotide polymorphisms (SNPs) in the NOS3, DDAH1, DDAH2, PRMT1, and AGXT2 genes were analyzed by PCR, and genotypes were related to biomarker levels and outcome. The primary outcome was the incidence of DCI, which was defined as the appearance of new infarctions on cranial computed tomography or magnetic resonance imaging. Results: 18 out of 51 SAH patients developed DCI. DCI patients did not significantly differ from those without DCI in clinical scores. However, patients who developed DCI had higher plasma ADMA and SDMA levels and higher SDMA levels in CSF at admission. DDAH1 gene variation was associated with plasma ADMA (p=0.02), whilst AGXT2 gene variation was associated with plasma SDMA (p=0.02). There was a strong association of all three DDAH1 SNPs that we analyzed with DCI, with carriers of the minor allele of DDAH1 rs233112 having a significantly increased relative risk of developing DCI (RR=2.61 (1.25-5.43), p=0.002). Conclusions: Sequence variation in the DDAH1 gene is associated with the incidence of DCI in SAH patients, suggesting that SNPs in the DDAH1 gene, which regulates plasma ADMA concentration, significantly influences the risk of cerebral ischemia after subarachnoid hemorrhage.

Associations between Early Hyperoxia and Long Term Neurologic Outcome in Acute Carbon Monoxide Poisoning

Purpose: We studied the impact of arterial oxygen tension (PaO2) on the long term neurologic outcome in patients with acute carbon monoxide poisoning. Methods: The study population included 311 patients who presented to emergency department with acute CO poisoning from January 2015 to January 2018. These patients underwent arterial blood gas testing at the time of presentation. The baseline demographic, clinical, laboratory, and clinical outcome data were recorded. The primary outcome of interest was the long term neurologic status. Results: The normoxia group was significantly older and it had a higher incidence of diffusion weighted MRI abnormality, and this group needed multiple HBO sessions compared to the group with moderate or severe hyperoxia. Also, the incidence of altered mentality at discharge was higher in the normoxia group than that of the moderate hyperoxia group. The incidence of a poor long term neurologic outcome was 11.3%. The incidence of a poor long term neurologic outcome decreased as the PaO2 increased. The PaO2 was significantly lower in patients with a poor long term neurologic outcome than that of the patients with a good outcome 198 (165.2 to 231.1) mmHg in the good outcome group vs. 154 (119-162) mmHg in poor outcome, p&lt;0.001). In multivariate logistic regression analysis, PaO2 was selected as an independent factor of the poor long-term neurologic outcome (OR 0.981 (95% CI: 0.968 to 0.995)) Conclusion: Higher PaO2 was independently associated with a lower incidence of a poor long-term neurologic outcome.

Is an increased PaO2 in a normobaric state safe in acute CO poisoning?

Our objective was to determine how much PaO2 levels increase after normobaric oxygen (NBO) therapy and whether NBO therapy exerts therapeutic effects regardless of the PaO2 level. We suggest the optimal PaO2 level to use during NBO therapy for the acute treatment of carbon monoxide (CO) poisoning. This retrospective study included 311 patients who received oxygen administration after CO poisoning and had a measurable PaO2 level upon arrival. Baseline characteristics, clinical courses and long-term neurological outcome were collected and compared. The PaO2 level upon arrival was 192 (161-225) mmHg, and 272 (87.5%) of the patients presented with hyperoxia. The incidence of poor long-term neurological outcome was 11.3% at a median follow-up period of 35months. PaO2 levels upon arrival were higher in patients with good long-term neurological outcome than in those with poor outcome. The incidence of poor long-term neurological outcome was significantly dependent on the PaO2 level when patients were stratified at 100-mmHg increments. A multivariate regression analysis showed that PaO2 levels, when considered a continuous, interval or ordinal variable, were associated with long-term neurological outcome in separate models. According to the three models, a PaO2 level of 200-300mmHg has the lowest risk of poor long-term neurological outcome. The results of the analysis of the predicted probability of poor long-term outcome according to the PaO2 level exhibited a U-shaped curve. Further large-scale studies are needed to confirm the association between 200-300mmHg of PaO2 and long-term neurological outcome and evaluate the impact of PaO2 levels above 300mmHg on acute CO poisoning outcome.

The predictive value of scores based on peripheral complete blood cell count for long-term neurological outcome in acute carbon monoxide intoxication.

Growing evidence indicates that inflammation is associated with neurological sequelae after CO poisoning. Several scores incorporating the peripheral complete blood cell (CBC) count have been introduced as indicators of systemic inflammation. This study investigated whether these scores can improve the predictive accuracy for long-term neurological outcome of acute carbon monoxide (CO) poisoning. Two hundred seventy-nine patients who suffered from acute CO poisoning were included. Data on the demographic details, serial peripheral CBC counts and scores based on peripheral CBC counts (neutrophil-lymphocyte ratio (NLR), monocyte-lymphocyte ratio (MLR), platelet-lymphocyte ratio (PLR), systemic immune inflammation index [SII]) over the first 12hours after presentation together with the clinical course during hospitalization and long-term neurological outcome were collected. Both a multivariate logistic regression model with only significant univariate predictors and a model with univariate predictors plus each score for long-term neurological outcome were constructed. Patients with a poor long-term neurological outcome had higher neutrophil and monocyte counts and lower lymphocyte counts over the first 12hours after admission than patients with a good outcome. The diagnostic performance of the NLR, MLR and SII over the first 12hours for predicting long-term neurological outcome was acceptable. These scores at presentation were independently associated with the long-term neurological outcome. Among these scores, only the SII at presentation significantly improved the predictive accuracy of the model when combined with clinical parameters (AUC 0.949, 95% CI 0.916-0.972 vs AUC 0.923, 95% CI 0.884-0.952 for the model with clinical parameters only, P=0.0476). The optimal cut-off value for SII at presentation was 1012.2, resulting in a sensitivity of 97% (84.2%-99.9%) and specificity of 64.6% (58.2%-70.6%). The SII at presentation could significantly improve the prognostic accuracy for predicting the long-term neurological outcome in patients with acute CO poisoning. Because the SII is an inexpensive and easily measurable parameter, it might be used as a prognostic tool in clinical fields.

Cerebral Near-Infrared Spectroscopy in Adult Patients Undergoing Veno-Arterial Extracorporeal Membrane Oxygenation.

Acute cerebral complications (ACC) of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) are associated with poor long-term neurologic outcome. We described the role of rSO2 monitoring in detecting ACC and desaturations and their relationship with poor outcome when employing VA-ECMO. Retrospective analysis of patients monitored by cerebral frontal near-infrared spectroscopy (NIRS) (CAS Medical Systems Inc., Branford, CT, USA) during VA-ECMO (November 2008-December 2015). ACC was defined as the presence of stroke and/or brain death, while cerebral desaturation as cortical oxygen tissue saturation (rSO2)<60%. Fifty-six of 159 VA-ECMO patients (age 55 [36-60] years) were included; 18 (32%) developed ACC and 36 died (64%). Cerebral desaturation occurred in 43 (74%) patients, who had a higher mortality than those without cerebral desaturation (74 vs. 31%). A high sequential organ failure assessment (SOFA) score on the first day of ECMO (OR 1.40 [95% CIs 1.06-1.84]) and the minimum ECMO blood flow during the first 4 days of therapy (OR 3.05 [1.01-9.17]) were independently associated with the occurrence of cerebral desaturation. Cerebral desaturation occurred more frequently in patients with ACC than others (94 vs. 68%); patients with ACC also had a lower minimal rSO2 over time (49 vs. 54%) and more frequently had high right-left rSO2 differences (33 vs. 8%), which were both independent predictors of ACC. The occurrence of cerebral desaturation (OR 7.93 [1.62-38.74]) and high lactate concentrations during the first 4 days of ECMO support (OR 1.22 [1.03-1.46]) was independently associated with hospital mortality. Monitoring of rSO2 could be considered as an interesting tool to monitor the brain of patients on VA-ECMO.

Serum N-terminal proBNP, not troponin I, at presentation predicts long-term neurologic outcome in acute charcoal-burning carbon monoxide intoxication

Objective: This study aimed to investigate whether the serum N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin I levels at emergency department (ED) presentation predict long-term neurologic outcomes after acute charcoal-burning carbon monoxide (CO) poisoning.Methods: This retrospective study included 220 patients suffering from charcoal-burning CO poisoning. The demographics, serum NT-proBNP and troponin I levels at ED presentation, treatment, clinical course during hospitalization, and long-term neurologic outcomes were collected.Results: The median serum NT-proBNP level at presentation was 48.8 (16.5–259) pg/mL, and 78 patients (35.5%) had elevated troponin I (>0.04 ng/mL) after acute charcoal-burning CO poisoning. The upper NT-proBNP and elevated troponin I groups had higher prevalences of respiratory failure, hypotension, and myocardial injury during hospitalization and altered mentality (GCS ≤14) at discharge than the lower NT-proBNP and normal troponin I groups. The incidence of persistent severe neurologic sequelae at 25 months after acute CO poisoning was 10.9%. The upper NT-proBNP and elevated troponin I groups had a higher incidence of poor long-term neurologic outcome than the counterpart groups. Log-transformed NT-proBNP and elevated troponin I were associated with poor long-term neurologic outcome in the univariate analysis, but only the adjusted log-transformed NT-proBNP remained an independent factor in the multivariate analysis. Compared with a predictive model including previously proposed predictors, the addition of log NT-proBNP improved the diagnostic accuracy for predicting poor long-term neurologic outcome. The serum NT-proBNP values for predicting poor long-term neurologic outcome were 74.6 and 32.7 pg/mL at fixed sensitivities of 95 and 99%, respectively.Conclusions: Elevated serum NT-proBNP at ED presentation is correlated with a risk of poor long-term neurologic outcome after discharge in cases of acute charcoal-burning CO poisoning. NT-proBNP could significantly improve the risk stratification of patients who will experience poor long-term neurologic outcome after CO poisoning. This potentially valuable marker should be further validated.

Initial diffusion-weighted MRI and long-term neurologic outcomes in charcoal-burning carbon monoxide poisoning

Context: This study assessed the results of diffusion-weighted imaging (DWI) at presentation for acute charcoal-burning carbon monoxide (CO) poisoning and investigated whether the initial DWI results can predict long-term neurologic outcomes.Methods: The study included 128 patients who suffered from CO poisoning after burning charcoal and underwent DWI. These patients were divided into two groups based on imaging results: a normal DWI group and an abnormal DWI group. Data regarding clinical courses and long-term neurologic outcomes (persistent severe neurologic sequelae) were collected and compared.Results: The rate of abnormal DWI findings at presentation was 23.4%, and the most common site of abnormalities was the globus pallidus. All lesions in abnormal DWI had decreased apparent diffusion coefficient (ADC) values. The long-term neurologic state was assessed at a median follow-up of 19.5 months, and the frequency of poor long-term neurologic outcome was significantly higher in the abnormal DWI group (40.0% in the abnormal DWI group vs. 1.0% in the normal DWI group; p < .001). Abnormal DWI (odds ratio [OR]): 31.3, 95% confidence interval [CI]: 2.5–397) and old age (OR 1.1, 95% CI: 1.001–1.13) were independent factors for poor long-term neurologic outcomes, whereas the Glasgow Coma Scale score at presentation (OR: 0.7, 95% CI: 0.6–0.9) was negatively associated with the risk of poor long-term neurologic outcome.Conclusions: In cases involving CO poisoning due to charcoal burning, DWI at presentation may help predict the long-term neurological outcome after discharge.

Status epilepticus: Having treatment paradigms in place in Neurosurgical settings

Status epilepticus (SE) is an emergency situation, which needs immediate and prompt treatment. Lack of early treatment often leads to permanent neuronal damage and poor long-term neurological outcome. Among the known neurosurgical causes of SE are central nervous system (CNS) tumors, subarachnoid and intracerebral hemorrhage (ICH), head trauma and post-operative states. Given the frequency of SE events in neurosurgical wards, it is essential that the neurosurgical teams and intensive care unit staff are adequately sensitized to the prompt detection and management of SE. Uniform, easily understandable and logical algorithms are needed as part of care pathways to enable satisfactory management. Such measures are imperative in improving long-term patient outcome.

Admission interleukin-6 is associated with post resuscitation organ dysfunction and predicts long-term neurological outcome after out-of-hospital ventricular fibrillation

Aim of the studyTo study plasma concentrations of interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP) and S-100B during intensive care after out-of-hospital cardiac arrest from ventricular fibrillation (OHCA-VF), and their associations with the duration of ischemia, organ dysfunction and long-term neurological outcome. Materials and methodsA 12-month prospective observational multicentre study was conducted in 21 Finnish intensive care units in 2011. IL-6, hs-CRP and S-100B were measured at 0–6h, 24h, 48h and 96h after ICU admission. Associations with the time to return of spontaneous circulation (ROSC), sequential organ failure assessment (SOFA) scores divided into tertiles and 12-month cerebral performance category (CPC) were tested. ResultsOf 186 OHCA-VF patients included in the study, 110 (59.1%) patients survived with good neurological outcome (CPC 1–2) 12 months after cardiac arrest. Admission plasma concentrations of IL-6 but not hs-CRP were higher with prolonged time to ROSC (p<0.001, 0.203, respectively), in patients with subsequent higher SOFA scores (p<0.001, 0.069) and poor long-term neurological outcome (CPC 3–5) (p<0.001, 0.315). S-100B concentrations over time were higher in patients with CPC of 3–5 (p<0.001). The area under the curve for prediction of poor 12-month outcome for admission levels was 0.711 IL-6, 0.663 for S-100B and 0.534 for hs-CRP. With multivariate logistic regression analysis only admission IL-6 (p=0.046, OR 1.006, 95% CI 1.000–1.011/ng/L) was an independent predictor of poor neurological outcome. ConclusionAdmission high IL-6, but not hs-CRP or S-100B, is associated with extra-cerebral organ dysfunction and along with age and time to ROSC are independent predictors for 12-month poor neurologic outcome (CPC 3–5).

Arteriopathy, D-Dimer, and Risk of Poor Neurologic Outcome in Childhood-Onset Arterial Ischemic Stroke

To assess whether acute findings of cerebral arteriopathy, large infarct, and acutely elevated plasma D-dimer levels are independently prognostic of poor long-term neurologic outcome as measured at ≥ 1 year post-event in children with arterial ischemic stroke (AIS). Sixty-one patients with childhood-onset (ie, >28 days of life) AIS were enrolled in a single-institution cohort study at Children's Hospital Colorado between February 2006 and June 2011. Data on demographic and diagnostic characteristics, antithrombotic treatments, and outcomes were systematically collected. Cerebral arteriopathy and D-dimer levels >500 ng/mL (a measure of coagulation activation) were identified acutely in 41% and 31% of the cohort, respectively. Anticoagulation was administered in the acute period post-event in 40% of the children, in the subacute period in 43%, and in the chronic period in 28%. When not receiving anticoagulation, patients were routinely treated with aspirin 2-5 mg/kg once daily for a minimum of 1 year. Death, major bleeding (including intracranial hemorrhage), and recurrent AIS were infrequent. The Pediatric Stroke Outcome Measure at 1 year demonstrated poor outcome in 54% of the children. Acute cerebral arteriopathy and elevated D-dimer level were identified as putative prognostic factors for poor outcome; after adjustment for D-dimer, arteriopathy was an independent prognostic indicator (OR, 19.0; 95% CI, 1.6-229.8; P = .02). Arteriopathy and coagulation activation are highly prevalent in the acute period of childhood AIS. Although recurrent AIS and intracranial hemorrhage were infrequent in our cohort, one-half of children experienced a poor neurologic outcome at 1 year, the risk of which was increased by acute arteriopathy. Substantiation of these findings in multi-institutional cohort studies is warranted, toward risk stratification in childhood-onset AIS.

An overview of risk factors for poor neurodevelopmental outcome associated with prematurity

Preterm birth is a major cause of neonatal mortality and morbidity. While advances in medical care have improved the survival of preterm infants, neurodevelopmental problems persist in this population. This article aims to review factors associated with their neurodevelopmental outcomes. English language studies of neurodevelopmental outcomes in preterm infants were retrieved from PubMed. A total of 100 related publications were included. Early gestational age and birth weight are the most significant predictors of poor long-term neurological outcome. Structural changes of the brain, infection, male gender and neonatal intensive care unit course are also important factors affecting eventual outcome. Other complex biological and socio-economic factors, which extend from prenatal through postnatal periods, up through and including adulthood, also affect the trajectory of brain development in preterm infants. Neurodevelopmental problems continue to affect the preterm population. There is a critical need for collaboration among geneticists, obstetricians, pediatricians, and neuroimaging and rehabilitation experts to determine early predictive factors and neuroprotective therapies to properly treat or prevent poor neurodevelopmental outcomes in these infants.

Cerebral Palsy and Assisted Conception

Assisted reproductive technologies have been widely used over the past 30 years, and 1% to 4% of births worldwide are products of these technologies. However, adverse health outcomes related to assisted reproductive technologies, including cerebral palsy, have been reported. We extracted and reviewed all relevant studies cited by Medline from 1996 to 2010 evaluating the role of assisted reproductive technologies as a causative factor for cerebral palsy and poor long-term neurologic outcome. The research suggests that multiple pregnancy, preterm delivery, and babies small for gestational age are factors in the development of cerebral palsy. The vanishing embryo syndrome may also play a role. We review the evidence for these potentially causative factors, as well as their implications for embryo transfer policies.

Update on diagnosis, treatment, and prognosis in opsoclonus–myoclonus–ataxia syndrome

Opsoclonus-myoclonus-ataxia syndrome (OMS) is a severe autoimmune central nervous system disorder, which predominantly affects young children and causes lifelong neurological disability. Early recognition and treatment may yield better outcomes. Appreciation of the spectrum of clinical presentations of OMS, awareness of common misdiagnoses, and utilization of diagnostic criteria may facilitate the timely diagnosis of OMS. Approximately 50% of patients have an associated neuroblastoma, which may escape detection by traditional methods and require MRI or computed tomography of the torso for diagnosis. In nonparaneoplastic cases, many associated infections have been reported. Although there has been progress in autoantibody identification and cerebrospinal fluid B cell expansion is a common finding, there is no diagnostic biomarker for OMS currently. Approximately 80% of reported patients, typically treated with conventional therapies such as adrenocorticotropin hormone, corticosteroids, and/or intravenous immunoglobulin, develop long-term neurological morbidity. Newer treatment approaches using early, aggressive therapy with cyclophosphamide or rituximab are promising. The diagnosis of OMS requires a high level of suspicion and a systematic approach for diagnostic testing, particularly for neuroblastoma. Future collaborative studies are required to determine whether early, aggressive therapy will improve the typically poor long-term neurological outcome.

Value of Cerebral Microhemorrhages Detected with Susceptibility-weighted MR Imaging for Prediction of Long-term Outcome in Children with Nonaccidental Trauma

To determine the prevalence of parenchymal brain microhemorrhages (MHs) in infants with nonaccidental trauma (NAT) by using susceptibility-weighted (SW) magnetic resonance (MR) imaging and to assess whether the presence of MH results in improved prediction of the long-term neurologic outcome. A retrospective case-control analysis of the data for 101 children aged 1-32 months with forensic pediatric specialist-confirmed NAT was performed with institutional review board approval. Sixty-two patients were boys (mean age, 8.4 months +/- 7.4 [standard deviation]), and 39 were girls (mean age, 7.4 months +/- 7.8). The imaging findings and clinical data of the children who were examined with SW imaging were collected. Exclusion criteria included pre-existing cognitive delays, central nervous system malformations, previous brain injuries, and/or birth before 30 weeks gestation. Dichotomized long-term neurologic outcomes (good [normal, mild disability, or moderate disability] versus poor [severe disability, vegetative state, or death]) at greater than or equal to 6 months (mean, 33 months; range 6-95 months) were available for 53 patients (36 boys [mean age, 7.3 months +/- 5.9]; 17 girls [mean age, 7.4 months +/- 7.9]; overall range, 2-32 months). Logistic regression was used to determine whether the presence of SW imaging-depicted MH, as compared with other radiologic findings, resulted in improved prediction of long-term neurologic outcome. Imaging findings showed that of the 101 patients, 29 (29%) had MH at SW imaging, 66 (65%) had extraaxial hemorrhages, 52 (51%) had retinal hemorrhages, and 35 (35%) had evidence of acute ischemic injury. A significantly larger number of children with poor outcomes than children with good outcomes had brain MH (nine of 14 vs seven of 39; P = .001) and ischemic injury (13 of 14 vs 17 of 39; P = .006). Logistic regression analysis revealed presence of MH at SW imaging-followed by acute ischemic injury, initial Glasgow Coma Scale score, and age-to be the most significant single variable in the final model, with an overall predictive accuracy of 92.5%. Presence of intraparenchymal brain MH in children with NAT, as detected on SW images, correlates with significantly poor long-term neurologic outcome, improves outcome prediction compared with the predictions made by using other tested clinical and imaging findings, and is most predictive when combined with presence of ischemic injury.

Automated respiratory support in newborn infants

A considerable proportion of premature infants requires mechanical ventilatory support and supplemental oxygen. Due to their immaturity, exposure to these forms of respiratory support contributes to the development of lung injury, oxidative stress and abnormal retinal development. These conditions are associated with poor long-term respiratory and neurological outcome. Mechanically ventilated preterm infants present with frequent fluctuations in ventilation and gas exchange. Currently available ventilatory modes and manual adjustment to the ventilator or supplemental oxygen cannot effectively adapt to these recurrent fluctuations. Moreover, the respiratory support often exceeds the infant's real needs. Techniques that adapt the mechanical ventilatory support and supplemental oxygen to the changing needs of preterm infants are being developed in order to improve stability of gas exchange, to minimise respiratory support and to reduce personnel workload. This article describes the preliminary evidence on the application of these new techniques in preterm infants and animal models.