Refractory Intracranial Hypertension in Posterior Reversible Encephalopathy Syndrome

Introduction

Posterior reversible encephalopathy syndrome (PRES) is a largely reversible disease with long-term favorable outcome. A minority of patients, however, may develop progressive cerebral edema and ischemia resulting in severe disability or death. We report a case of severe intracranial hypertension associated with PRES that was successfully treated according to intracranial pressure (ICP)- and cerebral perfusion pressure (CPP)-driven therapy.

Methods

Case report.

Results

A 42-year-old woman underwent bilateral lung transplantation for severe bronchiectasis. Her immunosuppressive regimen consisted of azathioprine, prednisone, and tacrolimus. She acutely developed an aggressive form of PRES that rapidly resulted in severe refractory intracranial hypertension despite discontinuation of potentially causative medications and adequate supportive therapy. Accordingly, second-tier therapies, including barbiturate infusion, were instituted and immunosuppression was switched to anti-thymocyte globulin followed by mycophenolate mofetil. Within 10 h of barbiturate administration, ICP dropped to 20 mmHg. Thiopental was administered for two days and then rapidly tapered because of severe urosepsis. Six months after discharge from the intensive care unit the patient returned to near-normal life, her only complaint being short-term amnesia.

Conclusions

The decision to undertake ICP monitoring in medical conditions in which no clear recommendations exist greatly relies on physicians’ judgment. This case suggests that ICP monitoring may be considered in the setting of acute PRES among selected patients, when severe intracranial hypertension is suspected, provided that a multidisciplinary team of neurocritical care specialists is readily available.     

Clinical correlates,outcomes and healthcare costs associated with early mechanical ventilation after kidney transplantation

Background

Information is lacking on the frequency, clinical implications, and costs of respiratory failure requiring mechanical ventilation after kidney transplantation.

Methods

US Renal Data System records for Medicare-insured kidney transplant recipients (1995 to 2007; n = 88,392) were examined to identify post-transplantation mechanical ventilation from billing claims within 30 days after transplantation.

Results

Post-transplantation mechanical ventilation was required among 2.1% of the cohort. Independent correlates of early mechanical ventilation included recipient age, low body mass index, coronary artery disease, and cerebrovascular disease. Post-transplantation mechanical ventilation was twice as likely with delayed graft function (adjusted odds ratio, 2.13; P < .001) and 35% lower among recipients of living versus deceased donor allografts. Patients needing early mechanical ventilation experienced 5-fold higher 1-year mortality, as well as significantly higher Medicare costs during the transplant hospitalization and first post-transplantation year.

Conclusions

Recognition of patients at risk for post-transplantation respiratory failure may help direct protocols for reducing the incidence and consequences of this complication.     

Costs of childhood asthma due to traffic-related pollution in two California communities

Recent research suggests the burden of childhood asthma that is attributable to air pollution has been underestimated in traditional risk assessments, and there are no estimates of these associated costs. We aimed to estimate the yearly childhood asthma-related costs attributable to air pollution for Riverside and Long Beach, CA, USA, including: 1) the indirect and direct costs of healthcare utilisation due to asthma exacerbations linked with traffic-related pollution (TRP); and 2) the costs of health care for asthma cases attributable to local TRP exposure. We calculated costs using estimates from peer-reviewed literature and the authors' analysis of surveys (Medical Expenditure Panel Survey, California Health Interview Survey, National Household Travel Survey, and Health Care Utilization Project). A lower-bound estimate of the asthma burden attributable to air pollution was US$18 million yearly. Asthma cases attributable to TRP exposure accounted for almost half of this cost. The cost of bronchitic episodes was a major proportion of both the annual cost of asthma cases attributable to TRP and of pollution-linked exacerbations. Traditional risk assessment methods underestimate both the burden of disease and cost of asthma associated with air pollution, and these costs are borne disproportionately by communities with higher than average TRP.     

Prevalence of viral respiratory tract infections in children with asthma

BACKGROUND: Previous studies support a strong association between viral respiratory tract infections and asthma exacerbations. The effect of newly discovered viruses on asthma control is less well defined. OBJECTIVE: We sought to determine the contribution of respiratory viruses to asthma exacerbations in children with a panel of PCR assays for common and newly discovered respiratory viruses. METHODS: Respiratory specimens from children aged 2 to 17 years with asthma exacerbations (case patients, n = 65) and with well-controlled asthma (control subjects, n = 77), frequency matched by age and season of enrollment, were tested for rhinoviruses, enteroviruses, respiratory syncytial virus, human metapneumovirus, coronaviruses 229E and OC43, parainfluenza viruses 1 to 3, influenza viruses, adenoviruses, and human bocavirus. RESULTS: Infection with respiratory viruses was associated with asthma exacerbations (63.1% in case patients vs 23.4% in control subjects; odds ratio, 5.6; 95% CI, 2.7- 11.6). Rhinovirus was by far the most prevalent virus (60% among case patients vs 18.2% among control subjects) and the only virus significantly associated with exacerbations (odds ratio, 6.8; 95% CI, 3.2-14.5). However, in children without clinically manifested viral respiratory tract illness, the prevalence of rhinovirus infection was similar in case patients (29.2%) versus control subjects (23.4%, P > .05). Other viruses detected included human metapneumovirus (4.6% in patients with acute asthma vs 2.6% in control subjects), enteroviruses (4.6% vs 0%), coronavirus 229E (0% vs 1.3%), and respiratory syncytial virus (1.5% vs 0%). CONCLUSION: Symptomatic rhinovirus infections are an important contributor to asthma exacerbations in children. CLINICAL IMPLICATIONS: These results support the need for therapies effective against rhinovirus as a means to decrease asthma exacerbations.     

Triple Therapy: When,if Ever?

Purpose of review

More than 9% of patients who undergo percutaneous coronary intervention (PCI) carry a concomitant indication for long-term anticoagulation (OAC). The optimal combination of anticoagulation and antiplatelet therapy for these patients remains uncertain.

Recent findings

Numerous studies have demonstrated that dual antiplatelet therapy (DAPT) remains superior to vitamin K antagonists (VKA) in the prevention of stent-related events. Nonetheless, OAC therapy is more efficacious than DAPT at reducing thromboembolism in patients with atrial fibrillation. The combination of DAPT and OAC, known as triple therapy, portends as much as a threefold increased risk of fatal and nonfatal bleeding compared to warfarin monotherapy. Recent studies have demonstrated the safety of shorter durations of triple therapy with subsequent transition to a P2Y₁₂ inhibitor in combination with an OAC.

Summary

Here, we review the evidence regarding the safety and efficacy of dual therapy with OAC in combination with a P2Y₁₂ inhibitor versus triple therapy among recently stented patients with a long-term requirement for OAC.

     

Association of Long-Term Exposure to Traffic-Related Air Pollution with Blood Pressure and Hypertension in an Adult Population–Based Cohort in Spain (the REGICOR Study)

Background: Long-term exposure to traffic-related air pollution may increase blood pressure (BP) and induce hypertension. However, evidence supporting these associations is limited, and they may be confounded by exposure to traffic noise and biased due to inappropriate control for use of BP-lowering medications.Objectives: We evaluated the associations of long-term traffic-related air pollution with BP and prevalent hypertension, adjusting for transportation noise and assessing different methodologies to control for BP-lowering medications.Methods: We measured systolic (SBP) and diastolic BP (DBP) at baseline (years 2003–2005) in 3,700 participants, 35–83 years of age, from a population-based cohort in Spain. We estimated home outdoor annual average concentrations of nitrogen dioxide (NO₂) with a land-use regression model. We used multivariate linear and logistic regression.Results: A 10-μg/m³ increase in NO₂ levels was associated with 1.34 mmHg (95% CI: 0.14, 2.55) higher SBP in nonmedicated individuals, after adjusting for transportation noise. Results were similar in the entire population after adjusting for medication, as commonly done, but weaker when other methods were used to account for medication use. For example, when 10 mmHg were added to the measured SBP levels of medicated participants, the association was β = 0.78 (95% CI: –0.43, 2.00). NO₂ was not associated with hypertension. Associations of NO₂ with SBP and DBP were stronger in participants with cardiovascular disease, and the association with SBP was stronger in those exposed to high traffic density and traffic noise levels ≥ 55 dB(A).Conclusions: We observed a positive association between long-term exposure to NO₂ and SBP, after adjustment for transportation noise, which was sensitive to the methodology used to account for medication.Citation: Foraster M, Basagaña X, Aguilera I, Rivera M, Agis D, Bouso L, Deltell A, Marrugat J, Ramos R, Sunyer J, Vila J, Elosua R, Künzli N. 2014. Association of long-term exposure to traffic-related air pollution with blood pressure and hypertension in an adult population–based cohort in Spain (the REGICOR study). Environ Health Perspect 122:404–411; http://dx.doi.org/10.1289/ehp.1306497