A Case of Amlodipine Overdose: Role of High Dose Insulin Therapy

Introduction: High dose insulin (HDI) therapy, defined as \u3e 0.5 units/kg/hour, has been postulated to improve hemodynamics in both calcium channel blocker (CCB) and beta-blocker overdose. Proposed benefits of HDI include coronary and systemic vasodilation due to enhancement of nitric oxide synthase activity leading to improved contractility and decreased systemic vascular resistance, respectively. HDI also directly improves cardiac contractility by increasing glucose uptake and improving calcium handling within cardiac cells. We present a case of a patient with amlodipine overdose and her response to HDI therapy. Case presentation: A 52 year old female presented with amlodipine overdose after suicide attempt leading to shock. She received continuous intravenous infusion of regular insulin at a rate of 2 units/kg/hour and epinephrine titrated up to 80 mcg/hour to maintain mean arterial pressure above 65. After several hours, there was concern for worsening hypokalemia so insulin was suspended. Patient subsequently became more hypotensive, requiring further uptitration of epinephrine. When continuous insulin was later restarted, there was an observed immediate improvement in blood pressure. Patient was eventually weaned off of vasopressors, followed by insulin, by day 3. She was downgraded from the ICU on day 5. Conclusion: In patients with CCB overdose, initial management should include fluid resuscitation, calcium supplementation, and early consideration of vasopressors and HDI therapy. Although there are currently no controlled human studies to evaluate the benefits of HDI therapy, this case revealed worsening hypotension upon cessation of therapy followed by rapid improvement in blood pressure when restarting insulin. Based on this observation, HDI therapy may have a prominent role in management of CCB overdose

Clinical features, antimicrobial susceptibility patterns and genomics of bacteria causing neonatal sepsis in a children's hospital in Vietnam: protocol for a prospective observational study.

INTRODUCTION: The clinical syndrome of neonatal sepsis, comprising signs of infection, septic shock and organ dysfunction in infants ≤4 weeks of age, is a frequent sequel to bloodstream infection and mandates urgent antimicrobial therapy. Bacterial characterisation and antimicrobial susceptibility testing is vital for ensuring appropriate therapy, as high rates of antimicrobial resistance (AMR), especially in low-income and middle-income countries, may adversely affect outcome. Ho Chi Minh City (HCMC) in Vietnam is a rapidly expanding city in Southeast Asia with a current population of almost 8 million. There are limited contemporary data on the causes of neonatal sepsis in Vietnam, and we hypothesise that the emergence of multidrug resistant bacteria is an increasing problem for the appropriate management of sepsis cases. In this study, we aim to investigate the major causes of neonatal sepsis and assess disease outcomes by clinical features, antimicrobial susceptibility profiles and genome composition. METHOD AND ANALYSIS: We will conduct a prospective observational study to characterise the clinical and microbiological features of neonatal sepsis in a major children's hospital in HCMC. All bacteria isolated from blood subjected to whole genome sequencing. We will compare clinical variables and outcomes between different bacterial species, genome composition and AMR gene content. AMR gene content will be assessed and stratified by species, years and contributing hospital departments. Genome sequences will be analysed to investigate phylogenetic relationships. ETHICS AND DISSEMINATION: The study will be conducted in accordance with the principles of the Declaration of Helsinki and the International Council on Harmonization Guidelines for Good Clinical Practice. Ethics approval has been provided by the Oxford Tropical Research Ethics Committee 35-16 and Vietnam Children's Hospital 1 Ethics Committee 73/GCN/BVND1. The findings will be disseminated at international conferences and peer-reviewed journals. TRIAL REGISTRATION NUMBER: ISRCTN69124914; Pre-results

An Outbreak of Severe Infections with Community-Acquired MRSA Carrying the Panton-Valentine Leukocidin Following Vaccination

Background: Infections with community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) are emerging worldwide. We investigated an outbreak of severe CA-MRSA infections in children following out-patient vaccination. Methods and Findings: We carried out a field investigation after adverse events following immunization (AEFI) were reported. We reviewed the clinical data from all cases. S. aureus recovered from skin infections and from nasal and throat swabs were analyzed by pulse-field gel electrophoresis, multi locus sequence typing, PCR and microarray. In May 2006, nine children presented with AEFI, ranging from fatal toxic shock syndrome, necrotizing soft tissue infection, purulent abscesses, to fever with rash. All had received a vaccination injection in different health centres in one District of Ho Chi Minh City. Eight children had been vaccinated by the same health care worker (HCW). Deficiencies in vaccine quality, storage practices, or preparation and delivery were not found. Infection control practices were insufficient. CA-MRSA was cultured in four children and from nasal and throat swabs from the HCW. Strains from children and HCW were indistinguishable. All carried the Panton-Valentine leukocidine (PVL), the staphylococcal enterotoxin B gene, the gene complex for staphylococcal-cassette-chromosome mec type V, and were sequence type 59. Strain HCM3A is epidemiologically unrelated to a strain of ST59 prevalent in the USA, althoughthey belong to the same lineage. Conclusions. We describe an outbreak of infections with CA-MRSA in children, transmitted by an asymptomatic colonized HCW during immunization injection. Consistent adherence to injection practice guidelines is needed to prevent CA-MRSA transmission in both in- and outpatient settings

Milrinone therapy for enterovirus 71-induced pulmonary edema and/or neurogenic shock in children: A randomized controlled trial

OBJECTIVE:: Enterovirus 71-induced brainstem encephalitis with pulmonary edema and/or neurogenic shock (stage 3B) is associated with rapid mortality in children. In a small pilot study, we found that milrinone reduced early mortality compared with historical controls. This prospective, randomized control trial was designed to provide more definitive evidence of the ability of milrinone to reduce the 1-week mortality of stage 3B enterovirus 71 infections. DESIGN:: Prospective, unicenter, open-label, randomized, controlled study. SETTING:: Inpatient ward of a large tertiary teaching hospital in Ho Chi Minh City, Vietnam. PATIENTS:: Children (≤18 yr old) admitted with proven enterovirus 71-induced pulmonary edema and/or neurogenic shock. INTERVENTIONS:: Patients were randomly assigned to receive intravenous milrinone (0.5 μg/kg/min) (n = 22) or conventional management (n = 19). Both groups received dopamine or dobutamine and intravenous immunoglobulin. MEASUREMENTS AND MAIN RESULTS:: The primary endpoint was 1-week mortality. The secondary endpoints included length of ventilator dependence and hospital stay and adverse events. The median age was 2 years with a predominance of boys in both groups. The 1-week mortality was significantly lower, 18.2% (4/22) in the milrinone compared with 57.9% (11/19) in the conventional management group (relative risk = 0.314 [95% CI, 0.12-0.83], p = 0.01). The median duration of ventilator-free days was longer in the milrinone treatment group (p = 0.01). There was no apparent neurologic sequela in the survivors in either group, and no drug-related adverse events were documented. CONCLUSIONS:: Milrinone significantly reduced the 1-week mortality of enterovirus 71-induced pulmonary edema and/or neurogenic shock without adverse effects. Further studies are needed to determine whether milrinone might be useful to prevent progression of earlier stages of brainstem encephalitis. Copyright © 2013 by the Society of Critical Care Medicine and Lippincott