Characterizing risk factors for pediatric lamp oil product exposures.

UNLABELLED: Poisonings from lamp oil ingestion continue to occur worldwide among the pediatric population despite preventive measures such as restricted sale of colored and scented lamp oils. This suggests that optimal prevention practices for unintentional pediatric exposures to lamp oil have yet to be identified and/or properly implemented. OBJECTIVE: To characterize demographic, health data, and potential risk factors associated with reported exposures to lamp oil by callers to poison centers (PCs) in the US and discuss their public health implications. STUDY DESIGN: This was a two part study in which the first part included characterizing all exposures to a lamp oil product reported to the National Poison Data System (NPDS) with regard to demographics, exposure, health, and outcome data from 1/1/2000 to 12/31/2010. Regional penetrance was calculated using NPDS data by grouping states into four regions and dividing the number of exposure calls by pediatric population per region (from the 2000 US census). Temporal analyses were performed on NPDS data by comparing number of exposures by season and around the July 4th holiday. Poisson regression was used to model the count of exposures for these analyses. In the second part of this project, in order to identify risk factors we conducted a telephone-based survey to the parents of children from five PCs in five different states. The 10 most recent lamp oil product exposure calls for each poison center were systematically selected for inclusion. Calls in which a parent or guardian witnessed a pediatric lamp oil product ingestion were eligible for inclusion. Data on demographics, exposure information, behavioral traits, and health were collected. A descriptive analysis was performed and Fisher's exact test was used to evaluate associations between variables. All analyses were conducted using SAS v9.3. RESULTS: Among NPDS data, 2 years was the most common patient age reported and states in the Midwestern region had the highest numbers of exposure calls compared to other regions. Exposure calls differed by season (p < 0.0001) and were higher around the July 4th holiday compared to the rest of the days in July (2.09 vs. 1.89 calls/day, p < 0.002). Most exposures occurred inside a house, were managed on-site and also had a "no effect" medical outcome. Of the 50 PC-administered surveys to parents or guardians, 39 (78%) met inclusion criteria for analysis. The majority of ingestions occurred in children that were 2 years of age, that were not alone, involved tiki torch fuel products located on a table or shelf, and occurred inside the home. The amount of lamp oil ingested did not appear to be associated with either the smell (p = 0.19) or the color of the oil (p = 1.00) in this small sample. Approximately half were asymptomatic (n = 18; 46%), and of those that reported symptoms, cough was the most common (n = 20, 95%) complaint. CONCLUSIONS: Lamp oil product exposures are most common among young children (around 2 years of age) while at home, not alone and likely as a result of the product being in a child-accessible location. Increasing parental awareness about potential health risks to children from these products and teaching safe storage and handling practices may help prevent both exposures and associated illness. These activities may be of greater benefit in Midwestern states and during summer months (including the period around the July 4th holiday).

Normal levels of cerebrospinal fluid hypocretin-1 and daytime sleepiness during attacks of relapsing-remitting multiple sclerosis and monosymptomatic optic neuritis.

There is emerging evidence that multiple sclerosis (MS), the hypothalamic sleep-wake regulating neuropeptide hypocretin-1 (hcrt-1) and the sleep disorder narcolepsy may be connected. Thus, the major pathophysiological component of narcolepsy is lack of hcrt-1. Dysfunction of the hypocretin system has been reported in MS case reports with attacks of hypothalamic lesions, undetectable cerebrospinal fluid (CSF) hcrt-1 and hypersomnia, but not found during remission in small samples. Finally, daytime sleepiness, the major symptom of narcolepsy, is reported in several MS populations, and there are case reports of co-existent narcolepsy and MS. However, it is unknown whether hcrt-1 and daytime sleepiness generally change during MS attacks. We therefore analyzed whether daytime sleepiness (using the Epworth Sleepiness Scale (ESS)) and CSF hcrt-1 levels differed between MS attack and remission, in 48 consecutively referred patients with relapsing-remitting MS (RRMS) or monosymptomatic optic neuritis (MON). Twenty-seven patients were in attack and 21 in remission. ESS was normal both during attacks (5.4 +/- 3.0) and remission (5.8 +/- 2.6), and mean CSF hcrt-1 was normal (456 +/- 41 pg/ml). No statistically significant differences were found between attack and remission. MRI scans revealed no hypothalamic lesions. The results show that the hypocretin system is intact and sleepiness is not typical in RRMS and MON without hypothalamic lesions on MRI.

Weight loss during chronic, cervical vagus nerve stimulation in depressed patients with obesity: an observation.

Fourteen patients were treated over 2 years with cervical vagus nerve stimulation (VNS) for adjunctive therapy of severe, treatment-resistant depression. Here, we report the serendipitous observation that this treatment was associated with highly significant, gradual weight loss despite the patients' report of not dieting or exercising. The weight loss was proportional to the initial BMI, that is, the more severe the obesity, the greater the weight loss. Weight loss did not correlate with changes in mood symptoms. The vagus nerve carries visceral information to and from the brain; modulation of its activity may alter eating behavior. Chronic cervical VNS may merit controlled study for the treatment of severe obesity.

An adolescent case of sulfhemoglobinemia associated with high-dose metoclopramide and N-acetylcysteine.

We describe the case of an adolescent girl who received high-dose metoclopramide in combination with oral N-acetylcysteine therapy for acute acetaminophen toxicity. Whole blood-sample analysis for abnormal hemoglobin pigments established the diagnosis of sulfhemoglobinemia. Metoclopramide has been shown to cause sulfhemoglobinemia, particularly when used in repeated high doses. Although N-acetylcysteine alone has not been associated as the cause, we suggest that sulfhemoglobine-mia is a potential complication in patients treated with metoclopramide for the nausea that often accompanies oral N-acetylcysteine therapy for acetaminophen toxicity. Cyanosis without respiratory distress should suggest this diagnosis.

Cardiovascular and endocrine responses to haemorrhage in the pig.

Heart rate (HR), mean arterial pressure (MAP), indices of sympathetic and parasympathetic activity (plasma concentrations of adrenaline, noradrenaline and pancreatic polypeptide, PP), vasopressin (VP) and aldosterone (ALDO) were measured in six pigs during continuous bleeding resulting in hypovolaemic shock, from which five survived. Three stages of haemorrhage could be defined. Stage I. Resting MAP was 85 +/- 6 mmHg and increased to 96 +/- 5 mmHg with a blood loss of 275 (range 250-300) (10 (9-12)% of the estimated blood volume) concomitant with an increase in HR from 105 +/- 5 to 113 +/- 6 beats min-1 (P less than 0.05). Stage II. After a blood loss of 375 (300-500) ml (15 (13-16)%) MAP fell to 62 +/- 9 mmHg and HR to 95 +/- 5 beats min-1 (P less than 0.05). Stage III. A blood loss of 1113 (825-1450) ml (44 (30-52)%) resulted in a MAP of 50 +/- 4 mmHg and an increase in HR to 206 +/- 3 beats min-1 (P less than 0.05). Adrenaline increased from 0.3 +/- 0.1 to 0.8 +/- 0.3 (stage II) and 3.6 +/- 1.1 nmol l-1 (stage III) (P less than 0.05); noradrenaline from 0.4 +/- 0.1 to 1.5 +/- 0.4 (stage II) and 5.9 +/- 1.7 nmol l-1 (stage III) (P less than 0.05); PP from 6.2 +/- 1.6 to 13.3 +/- 2.3 (stage II) and 20.9 +/- 7.8 pmol l-1 (stage III) (P less than 0.05). VP changed only marginally, but ALDO increased from 496 +/- 54 to 623 +/- 76 pmol l-1 (stage III) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Regional distribution of neuropeptide Y and its receptor in the porcine central nervous system.

The regional distribution of neuropeptide Y (NPY) immunoreactivity and receptor binding was studied in the porcine CNS. The highest amounts of immunoreactive NPY were found in the hypothalamus, septum pellucidum, gyrus cinguli, cortex frontalis, parietalis, and piriformis, corpus amygdaloideum, and bulbus olfactorius (200-1,000 pmol/g wet weight). In the cortex temporalis and occipitalis, striatum, hippocampus, tractus olfactorius, corpus mamillare, thalamus, and globus pallidus, the NPY content was 50-200 pmol/g wet weight, whereas the striatum, colliculi, substantia nigra, cerebellum, pons, medulla oblongata, and medulla spinalis contained less than 50 pmol/g wet weight. The receptor binding of NPY was highest in the hippocampus, corpus fornicis, corpus amygdaloideum, nucleus accumbens, and neurohypophysis, with a range of 1.0-5.87 pmol/mg of protein. Intermediate binding (0.5-1.0 pmol/mg of protein) was found in the septum pellucidum, columna fornicis, corpus mamillare, cortex piriformis, gyrus cinguli, striatum, substantia grisea centralis, substantia nigra, and cerebellum. In the corpus callosum, basal ganglia, corpus pineale, colliculi, corpus geniculatum mediale, nucleus ruber, pons, medulla oblongata, and medulla spinalis, receptor binding of NPY was detectable but less than 0.5 pmol/mg of protein. No binding was observed in the bulbus and tractus olfactorius and adenohypophysis. In conclusion, immunoreactive NPY and its receptors are widespread in the porcine CNS, with predominant location in the limbic system, olfactory system, hypothalamoneurohypophysial tract, corpus striatum, and cerebral cortex.