Nurse-Initiated Protocol to Improve Timely Antibiotic Administration in Pediatric Open Fractures.

BACKGROUND: Early administration of antibiotics in the presence of open fractures is critical in reducing infections and later complications. Current guidelines recommend administering antibiotics within 60 min of patient arrival to the emergency department, yet trauma centers often struggle to meet this metric. OBJECTIVES: This study aims to evaluate the impact of a nurse-initiated evidence-based treatment protocol on the timeliness of antibiotic administration in pediatric patients with open fractures. METHODS: A retrospective pre-post study of patients who met the National Trauma Data Standard registry inclusion criteria for open fractures of long bones, amputations, or lawn mower injuries was performed at a Midwestern United States Level II pediatric trauma center. The time of patient arrival and time of antibiotic administration from preimplementation (2015-2020) to postimplementation (2021-2022) of the protocol were compared. Patients transferred in who received antibiotics at an outside facility were excluded. RESULTS: A total of N = 73 participants met the study inclusion criteria, of which n = 41 were in the preimplementation group and n = 32 were in the postimplementation group. Patients receiving antibiotics within 60 min of arrival increased from n = 24/41 (58.5%) preimplementation to n = 26/32 (84.4%) postimplementation (p< .05). CONCLUSIONS: Our study demonstrates that initiating evidence-based treatment orders from triage helped decrease the time from arrival to time of antibiotic administration in patients with open fractures. We sustained improvement for 24 months after the implementation of our intervention.

Acute Hemorrhagic Edema of Infancy With Associated Hemorrhagic Lacrimation.

ABSTRACT: Acute hemorrhagic edema of infancy is a rare leukocytoclastic vasculitis that affects infants and children aged 4 to 24 months. We report a case of a 5-month-old girl with purpuric lesions with associated hemorrhagic lacrimation and epistaxis.

A Quality Improvement Initiative to Improve the Administration of Systemic Corticosteroids in the Pediatric Emergency Department.

INTRODUCTION: Timely administration of corticosteroids improves asthma care in the pediatric emergency department (ED). Using the Model for Improvement, we aimed to decrease time to delivery of corticosteroids in patients presenting to the ED with an acute asthma exacerbation. METHODS: This is a single-center, prospective, multidisciplinary quality improvement (QI) project targeting ED patients 1-18 years of age with an acute asthma exacerbation. We collected 5 months of baseline data from the arrival time of an ED patient with an asthma exacerbation with a Modified Pulmonary Index Score ≥5 to the time of administration of corticosteroids. A quality improvement project was launched in October 2017 involving multiple Plan-Do-Study-Act ramps. Improvement interventions continued for 9 months through June 2018, including reeducation of residents and nurses in the ED asthma order set and nursing treatment protocols, respectively, and changes to the electronic health record. Data were tacked for 15 additional months until September 2019. To promote the use of the nursing treatment protocol, we utilized real-time improvement feedback and continuing nursing education. RESULTS: The mean percentage of patients receiving steroids within 60 minutes of arrival improved from 59.3% to 84.3% over the first 5 months. The mean time to the administration of steroids within 60 minutes of arrival improved from 71.4 to 48.1 minutes. There was no increase in ED return rates. CONCLUSIONS: Our project improved the percentage of patients with acute asthma exacerbations receiving steroids within 60 minutes of ED arrival and mean time to administration of steroids. We sustained improvement for 18 months after the implementation of our QI interventions.

Differentiating non-responders from responders in children with moderate and severe asthma exacerbations.

Objective: Our goal was to assess factors associated with non-response to treatment in children presenting to the Emergency Department (ED) with moderate and severe asthma exacerbations. Methods: A retrospective chart review was completed from 9/2014 to 2/2017 for patients with a discharge diagnosis of asthma exacerbation. The Modified Pulmonary Index Score (MPIS) was used to quantify illness acuity. The rate of change of MPIS per hour was calculated, and differentiated responders from non-responders. After examining a histogram of ΔMPIS/h, a threshold of ΔMPIS/h > 0 was used to define response for duration of ED stay. Children included were >2 years and had initial MPIS > 10. Results: Eight hundred and fifty-two children were included. There were 178 (21%) non-responders and 674 (79%) responders. Non-responders were significantly older (7.0 ± 4.0 versus 5.6 ± 3.2 years; p < 0.001), but there were no differences in gender, race, ethnicity or insurance status. There was also no statistical difference in time to first albuterol treatment (50 ± 41 versus 43 ± 40 min; p = 0.05), or in time to corticosteroid (95 ± 75 versus 79 ± 64 min; p = 0.06). Non-responders were significantly more likely to arrive by ambulance (OR 2.2; 95% CI 1.6-3.2), to be admitted to the hospital (OR 2.7; 95% CI 1.8-4.0), and to be admitted to the ICU (OR 5.0; 95% CI 3.1-8.1). Conclusions: One in five children with exacerbations did not respond to treatment. These children were older and more likely to be admitted. Non-measured factors, possibly genetic, may contribute to response to treatment.

Lemierre's Syndrome Presenting as Multifocal Pyomyositis in a Young Child.

Lemierre's syndrome is more common in young adults and the majority of patients present with pharyngitis. Multifocal pyomyositis is very rare in this setting and in young children. We present here a case of multifocal pyomyositis caused by Fusobacterium spp. in a young child. Fusobacterium should be considered in the differential diagnosis of multifocal pyomyositis of unclear etiology.

Modulation of innate immunity by copolymer-1 leads to neuroprotection in murine HIV-1 encephalitis.

Virus-infected and immune-competent mononuclear phagocytes (MP; perivascular macrophages and microglia) drive the neuropathogenesis of human immunodeficiency virus type 1 (HIV-1) infection. Modulation of the MP phenotype from neurodestructive to neuroprotective underlies adjunctive therapeutic strategies for human disease. We reasoned that, as Copolymer-1 (Cop-1) can induce neuroprotective activities in a number of neuroinflammatory and neurodegenerative disorders, it could directly modulate HIV-1-infected MP neurotoxic activities. We now demonstrate that, in laboratory assays, Cop-1-stimulated virus-infected human monocyte-derived macrophages (MDM) protect against neuronal injury. Severe combined immune-deficient (SCID) mice were stereotactically injected with HIV-1-infected human MDM, into the basal ganglia, to induce HIV-1 encephalitis (HIVE). Cop-1 was administered subcutaneously for 7 days. In HIVE mice, Cop-1 treatment led to anti-inflammatory and neuroprotective responses. Reduced micro- and astrogliosis, and conserved NeuN/MAP-2 levels were observed in virus-affected brain regions in Cop-1-treated mice. These were linked to interleukin-10 and brain-derived neurotrophic factor expression and downregulation of inducible nitric oxide synthase. The data, taken together, demonstrate that Cop-1 can modulate innate immunity and, as such, improve disease outcomes in an animal model of HIVE.

Copolymer-1 induces adaptive immune anti-inflammatory glial and neuroprotective responses in a murine model of HIV-1 encephalitis.

Copolymer-1 (COP-1) elicits neuroprotective activities in a wide range of neurodegenerative disorders. This occurs, in part, by adaptive immune-mediated suppression of microglial inflammatory responses. Because HIV infection and immune activation of perivascular macrophages and microglia drive a metabolic encephalopathy, we reasoned that COP-1 could be developed as an adjunctive therapy for disease. To test this, we developed a novel animal model system that reflects HIV-1 encephalitis in rodents with both innate and adaptive arms of the immune system. Bone marrow-derived macrophages were infected with HIV-1/vesicular stomatitis-pseudotyped virus and stereotactically injected into the basal ganglia of syngeneic mice. HIV-1 pseudotyped with vesicular stomatitis virus envelope-infected bone marrow-derived macrophages induced significant neuroinflammation, including astrogliosis and microglial activation with subsequent neuronal damage. Importantly, COP-1 immunization reduced astro- and microgliosis while diminishing neurodegeneration. Hippocampal neurogenesis was, in part, restored. This paralleled reductions in proinflammatory cytokines, including TNF-alpha and IL-1beta, and inducible NO synthase, and increases in brain-derived neurotrophic factor. Ingress of Foxp3- and IL-4-expressing lymphocytes into brains of COP-1-immunized animals was observed. We conclude that COP-1 may warrant therapeutic consideration for HIV-1-associated cognitive impairments.

Human immunodeficiency virus type 1 pathobiology studied in humanized BALB/c-Rag2-/-gammac-/- mice.

The specificity of human immunodeficiency virus type 1 (HIV-1) for human cells precludes virus infection in most mammalian species and limits the utility of small animal models for studies of disease pathogenesis, therapy, and vaccine development. One way to overcome this limitation is by human cell xenotransplantation in immune-deficient mice. However, this has proved inadequate, as engraftment of human immune cells is limited (both functionally and quantitatively) following transplantation of mature human lymphocytes or fetal thymus/liver. To this end, a human immune system was generated from umbilical cord blood-derived CD34(+) hematopoietic stem cells in BALB/c-Rag2(-/-)gamma(c)(-/-) mice. Intrapartum busulfan administration followed by irradiation of newborn pups resulted in uniform engraftment characterized by human T-cell development in thymus, B-cell maturation in bone marrow, lymph node development, immunoglobulin M (IgM)/IgG production, and humoral immune responses following ActHIB vaccination. Infection of reconstituted mice by CCR5-coreceptor utilizing HIV-1(ADA) and subtype C 1157 viral strains elicited productive viral replication and lymphadenopathy in a dose-dependent fashion. We conclude that humanized BALB/c-Rag2(-/-)gamma(c)(-/-) mice represent a unique and valuable resource for HIV-1 pathobiology studies.