Enhancing Diagnostic Follow-up and Care Coordination for Children with Autism in a Busy Resident Continuity Clinic: Leveraging the Electronic Health Record.

PURPOSE: A high-quality primary care clinic should provide clear action points and important care coordination for a child receiving a new diagnosis of autism spectrum disorder (ASD). Unfortunately, a substantial proportion of caregivers report little-to-no post-diagnosis support from their home clinics and primary care providers often report lack of training and resources in providing these supports. METHODS: We implemented an intervention package to investigate the impact on the frequency and quality of follow-up care for children with ASD in a busy, high-volume resident continuity clinic. The package consisted of a care coordination scheduling pathway and a standardized clinical template-embedded in the electronic health record (EHR)-that guided providers through best-practice recommendations and patient resources. RESULTS: As a result of these interventions, 74% of patients had ASD-specific follow-up, a more than threefold increase from baseline with a majority of providers using the EHR-embedded template to guide their visit. Providers also indicated a high degree of usability for the system and that it aided them in following best-practice guidelines for ASD care. CONCLUSION: Through explicit scheduling pathways and a novel EHR template, we saw a significant increase in ASD-specific follow-up visits and implementation of best practices for ASD care, demonstrating a new process for training and engaging primary care providers in clear action steps for post-diagnostic care without having to rely on tertiary referrals.

TNF-α type 2 receptor mediates renal inflammatory response to chronic angiotensin II administration with high salt intake in mice.

Tumor necrosis factor-alpha (TNF-α) has been implicated in salt-sensitive hypertension and renal injury (RI) induced by angiotensin II (ANG II). To determine the receptor type of TNF-α involved in this mechanism, we evaluated the responses to chronic ANG II infusion (25 ng/min by implanted minipump) given with high-salt diet (HS; 4% NaCl) for 2 wk in gene knockout mice for TNF-α receptor type 1 (TNFR1KO; n = 6) and type 2 (TNFR2KO; n = 6) and compared the responses with those in wild-type (WT; C57BL/6; n = 6) mice. Blood pressure in these mice was measured by implanted radiotelemetry as well as by tail-cuff plethysmography. RI responses were assessed by measuring macrophage cell infiltration (CD68(+) immunohistochemistry), glomerulosclerosis (PAS staining), and interstitial fibrosis (Gomori's trichrome staining) in renal tissues at the end of the treatment period. The increase in mean arterial pressure induced by ANG II + HS treatment was not different in these three groups of mice (TNFR1KO, 114 ± 1 to 161 ± 7 mmHg; TNFR2KO, 113 ± 1 to 161 ± 3 mmHg; WT, 110 ± 3 to 154 ± 3 mmHg). ANG II + HS-induced RI changes were similar in TNFR1KO mice but significantly less in TNFR2KO mice (macrophage infiltration, 0.02 ± 0.01 vs. 1.65 ± 0.45 cells/mm(2); glomerulosclerosis, 26.3 ± 2.6 vs. 35.7 ± 2.2% area; and interstitial fibrosis, 5.2 ± 0.6 vs. 8.1 ± 1.1% area) compared with the RI changes in WT mice. The results suggest that a direct activation of TNF-α receptors may not be required in inducing hypertensive response to chronic ANG II administration with HS intake, but the induction of inflammatory responses leading to renal injury are mainly mediated by TNF-α receptor type 2.