2013 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report

ABSTRACT Background: This is the 31st Annual Report of the American Association of Poison Control Centers’ (AAPCC) National Poison Data System (NPDS). As of January 1, 2013, 57 of the nation's poison centers (PCs) uploaded case data automatically to NPDS. The upload interval was 8.08 [7.10, 11.63] (median [25%, 75%]) minutes, creating a near real-time national exposure and information database and surveillance system. Methodology: We analyzed the case data tabulating specific indices from NPDS. The methodology was similar to that of previous years. Where changes were introduced, the differences are identified. Poison center (PC) cases with medical outcomes of death were evaluated by a team of 38 medical and clinical toxicologist reviewers using an ordinal scale of 1–6 to assess the Relative Contribution to Fatality (RCF) of the exposure to the death. Results: In 2013, 3,060,122 closed encounters were logged by NPDS: 2,188,013 human exposures, 59,496 animal exposures, 806,347 information calls, 6,116 human-confirmed nonexposures, and 150 animal-confirmed nonexposures. Total encounters showed a 9.3% decline from 2012, while health care facility human exposure calls were essentially flat, decreasing by 0.1%.All information calls decreased 21.4% and health care facility (HCF) information calls decreased 8.5%, medication identification requests (drug ID) decreased 26.8%, and human exposures reported to US PCs decreased 3.8%. Human exposures with less serious outcomes have decreased 3.7% per year since 2008 while those with more serious outcomes (moderate, major or death) have increased by 4.7% per year since 2000. The top five substance classes most frequently involved in all human exposures were analgesics (11.5%), cosmetics/personal care products (7.7%), household cleaning substances (7.6%), sedatives/hypnotics/antipsychotics (5.9%), and antidepressants (4.2%). Sedative/hypnotics/antipsychotics exposures as a class increased most rapidly (2,559 calls/year) over the last 13 years for cases showing more serious outcomes. The top five most common exposures in children of 5 years or less were cosmetics/personal care products (13.8%), household cleaning substances (10.4%), analgesics (9.8%), foreign bodies/toys/miscellaneous (6.9%), and topical preparations (6.1%). Drug identification requests comprised 50.7% of all information calls. NPDS documented 2,477 human exposures resulting in death with 2,113 human fatalities judged related (RCF of 1, undoubtedly responsible; 2, probably responsible; or 3, contributory). Conclusions: These data support the continued value of PC expertise and need for specialized medical toxicology information to manage the more severe exposures, despite a decrease in calls involving less severe exposures. Unintentional and intentional exposures continue to be a significant cause of morbidity and mortality in the United States. The near real-time, always current status of NPDS represents a national public health resource to collect and monitor US exposure cases and information calls. The continuing mission of NPDS is to provide a nationwide infrastructure for public health surveillance for all types of exposures, public health event identification, resilience response and situational awareness tracking. NPDS is a model system for the nation and global public health.


Introduction
This is the 31st Annual Report of the American Association of Poison Control Centers ' (AAPCC; http://www.aapcc. org) National Poison Data System (NPDS).(1) On 1 January 2013, fi fty-seven regional poison centers (PCs) serving the entire population of the 50 United States, American Samoa, District of Columbia, Federated States of Micronesia, Guam, Puerto Rico, and the US Virgin Islands submitted information and exposure case data collected during the course of providing telephonic patient-tailored exposure management and poison information.
NPDS is the data warehouse for the nation ' s 57 PCs. PCs place emphasis on exposure management, accurate data collection and coding, and responding to the continuing need for poison related public and professional education. The PC ' s health care professionals are available free of charge to users, 24-hours a day, every day of the year. PCs respond to questions from the public, health care professionals, and public health agencies. The continuous staff dedication at the PCs is manifest as the number of exposure, and information call encounters exceeds 3.0 million annually. PC encounters involve either an exposed human or animal (EXPOSURE CALL) or a request for information with no person or animal exposed to any foreign body, viral, bacterial, venomous, or chemical agent or commercial product (INFORMATION CALL).

The NPDS Products Database
The NPDS products database contains over 400,000 products ranging from viral and bacterial agents to commercial chemical and drug products. The product database is maintained and continuously updated by data analysts at the Micromedex Poisindex ® System (Micromedex Healthcare Series [Internet database]; Greenwood Village, CO: Truven Health Analytics). A robust generic coding system categorizes the products data into 1,081 generic codes. These generic codes collapse into Nonpharmaceutical (562) and Surveillance defi nitions can be created to monitor a variety of volume parameters or case-based defi nitions on any desired substance or commercial product in the Micromedex Poisindex products database and/or set of clinical effects or other parameters. The products database contains over 400,000 entries. Surveillance defi nitions may be constructed using volume or case-based defi nitions with a variety of mathematical options and historical baseline periods from 1 to 13 years. NPDS surveillance tools include the following: Incoming data are monitored continuously and anomalous signals generate an automated email alert to the AAPCC ' s surveillance team or designated PC or public health agency staff. These anomaly alerts are reviewed daily by the AAPCC surveillance team, the PC, or the public health agency that created the surveillance defi nition. When reports of potential public health signifi cance are detected, additional information is obtained via the NPDS surveillance correspondence system or phone as appropriate from reporting PCs. The PC then alerts their respective state or local health departments.

Information Calls to Poison Centers
Data from 806,347 information calls to PCs in 2013 (Table 1C) was transmitted to NPDS, including calls in optional reporting categories such as prevention/safety/education (24,249), administrative (25,878), and caller referral (47,682). Figure 2 shows that all drug ID calls decreased dramatically in mid-2009, again in late 2010 and late 2011, and continue to decrease in 2012 and 2013. Law enforcement drug ID calls also showed a decline. The most frequent information call was for drug ID, comprising 408,711calls to PCs during the year. Of these, 239,364 (58.6%) were identifi ed as drugs with known abuse potential; however, these cases were categorized based on the drug ' s abuse potential without any knowledge of whether abuse was actually intended.
While the number of drug information calls decreased 21. 4% from 2012 (144,267 calls) to 2013 (113,378 calls), the distribution of these call types remained steady at 14.1% of all information request calls. The most common drug information requests were about drug -drug interactions, followed by other drug information, therapeutic use and indications, questions about dosage, and inquiries of adverse effects. Environmental inquiries comprised 2.3% of all information calls. Of these environmental inquiries, specifi c questions related to cleanup of mercury (thermometers and other) remained the most common followed by questions involving pesticides.
Of all the information calls, poison information comprised 7.0% of the requests with inquiries involving general toxicity the most common followed by questions involving food preparation practices, safe use of household products, and plant toxicity.

Exposure Calls to Poison Centers
In 2013, the participating PCs logged 3,060,122 total encounters including 2,188,013 closed human exposure cases (Table 1A), 59,496 animal exposures (Table 1B), 806,347 information calls (Table 1C), 6,116 human confi rmed non- Table 1A. AAPCC Population Served andReported Exposures (1983 -2013 Figure 1 shows the human exposures, information calls and animal exposures by day since 1 January 2001. Secondorder (quadratic) least squares regression of these data shows a statistically signifi cant departure from linearity (declining rate of calls since mid-2007) for human exposure calls. Information calls are best described by a smoothing spline fi t, and animal exposure calls have likewise been declining since mid-2005.
A hallmark of PC case management is the use of follow-up calls to monitor case progress and medical outcome. US PCs made 2,515,811 follow-up calls in 2013. Follow-up calls were made in 46.1% of human exposure cases. One follow-up call was made in 22.0% of human exposure cases, and multiple follow-up calls (range, 2 -121) were placed in 24.1% of cases. Figure 3 shows a graphic summary and analyses of Health Care Facility (HCF) exposure and HCF information calls. HCF exposure calls slightly departed from linearity but continued to increase at a steady rate, while the rate of HCF information calls has been declining since early 2005. This increasing use of the PCs for the more serious exposures (HCF calls) is important in the face of the decline in exposure and information calls. The 2 May 2006 exposure data spike on the fi gure was the result of 602 children in a Midwest school reporting a noxious odor which caused anxiety, but resolved without sequelae.
Tables 22A (Nonpharmaceuticals) and 22B (Pharmaceuticals) provide summary demographic data on patient age, reason for exposure, medical outcome, and use of a health care facility for all 2,188,013 human exposure cases, presented by substance categories. The Pharmaceuticals category includes both licit and illicit drugs.
Column 1: Name of the major, minor generic categories and their associated generic codes.
Column 2: Number of Case Mentions (All Exposures) in grey shading, displays the number of times the specifi c generic code was reported in all human exposure cases. If a human exposure case has multiple instances of a specifi c generic code, it is counted only once.
Column 3: Single Substance Exposures; this column was previously named " No. of Single Exposures " and was renamed in the 2009 report for clarity. This column displays the number of human exposure cases that identifi ed only one substance (one case, one substance).
The succeeding columns (Age, Reason, Treatment Site, And Outcome) show selected detail from these single-substance exposure cases. Death cases include both cases that have the outcomes of Death or Death (indirect report).These death cases are not limited by the relative contribution to fatality.
Tables 22A and 22B restrict the breakdown columns to single-substance cases. Prior to 2007, when multisubstance exposures were included, a relatively innocuous substance could be mentioned in a death column when, for example,  the death was attributed to an antidepressant, opioid, or cyanide. This subtlety was not always appreciated by the user of this table. The restriction of the breakdowns to singlesubstance exposures should increase precision and reduce misrepresentation of the results in this unique by-substance table. Single-substance cases refl ect the majority (89.1%) of all exposures. In contrast, only 44.2% of fatalities are single substance exposures (Table 5). Tables 22A and 22B tabulate 2,575,837 substance exposures, of which 1,950,455 were single-substance exposures, including1,013,229 (52.0%) nonpharmaceuticals and 937,226 (48.0%) pharmaceuticals. In 19.6% of singlesubstance exposures that involved pharmaceutical substances, the reason for exposure was intentional, compared with only 3.6% that involved a nonpharmaceutical substance. Correspondingly, treatment in a health care facility was provided in a higher percentage of exposures that   AAPCC 2013 Annual Report of the NPDS 1047 duration ( n ϭ 6,830), 31.5% occurred in the fi rst trimester, 37.0% in the second trimester, and 31.5% in the third trimester. Most (73.9%) were unintentional exposures and 19.6% were intentional exposures. There was one death of a pregnant woman in 2013.

Chronicity
Most human exposures, 1,922,316 (87.9%), were acute cases (single, repeated, or continuous exposure occurring over 8 hours or less) compared with 1,328 acute cases of 2,477 fatalities (53.6%). Chronic exposures (continuous or repeated exposures occurring over Ͼ 8 hours) comprised 2.1% (46,900) of all human exposures. Acute-on-chronic exposures (single exposure that was preceded by a continuous, repeated, or intermittent exposure occurring over a period of Ͼ 8 hours) numbered 188,899 (8.6%).

Scenarios
Of the total 289,699 therapeutic errors, the most common scenarios for all ages included: inadvertent double dosing  Table 3A) b AAPCC Total as of 1 July 2013 320,169,863 (see Table 1A). ( 3,4,5)  a Age includes cases with both actual and estimated ages as shown in Table 21. b Includes cases with relative contribution to fatality of 1 -undoubtedly responsible, 2 -probably responsible, or 3 -contributory. This excludes reports with outcome of Death INDIRECT. (28.2%), wrong medication taken or given (16.2%), other incorrect dose (13.6%), doses given/taken too close together (10.3%), and inadvertent exposure to someone else ' s medication (8.0%). The types of therapeutic errors observed are different for each age group and are summarized in Table 6B.

Reason by Age
Intentional exposures accounted for 16.2% of human exposures. Suicidal intent was suspected in 10.5% of cases, intentional misuse in 2.5%, and intentional abuse in 2.2%. Unintentional exposures outnumbered intentional exposures in all age groups with the exception of ages 13 -19 years (Table 7). Intentional exposures were more frequently reported than unintentional exposures in patients aged 13 -19 years. In contrast, of the 1,218 reported fatalities with RCF 1 -3, the major reason reported for children Յ 5 years was unintentional while most fatalities in adults ( Ͼ 20 years) were intentional ( Table 8).

Clinical Effects
The NPDS database allows for the coding of up to 131 individual clinical effects (signs, symptoms, or laboratory abnormalities) for each case. Each clinical effect can be further defi ned as related, not related, or unknown if related. Clinical effects were coded in 810,259 (37.0%) cases (17.8%  Table 11 displays the medical outcome of human exposure cases distributed by age. Older age groups exhibit a greater number of severe medical outcomes. Table 12 compares medical outcome and reason for exposure, and shows a greater frequency of serious outcomes in intentional exposures.

Medical Outcome
The duration of effect is required for all cases which report at least one clinical effect and have a medical outcome of minor, moderate, or major effect ( n ϭ 503,501; 23.0% of exposures). Table 13 demonstrates an increasing duration of the clinical effects observed with more severe outcomes.

Decontamination Procedures and Specifi c Antidotes
Tables 14 and 15 outline the use of decontamination procedures, specifi c physiological antagonists (antidotes), and measures to enhance elimination in the treatment of patients reported in the NPDS database. These should be interpreted as minimum frequencies because of the limitations of telephone data gathering.
Ipecac-induced emesis for poisoning continues to decline as shown in Tables 16A and 16B. Ipecac was administered in only 42 (0.0%) of pediatric exposures in 2013. The continued decrease in ipecac syrup use over the last 2 decades is likely a result of ipecac use guidelines issued in 1997 by the American Academy of Clinical Toxicology and the European Association of Poisons Centres and Clinical Toxicologists and updated in 2004.(6,7) In a separate report, the American Academy of Pediatrics not only concluded that ipecac should no longer be used routinely as a home treatment strategy, but also recommended disposal of home ipecac stocks.(8) A decline was also observed since the early 1990s for reported use of activated charcoal. While not as more serious outcomes (moderate, severe, and death). This ranking provides an indication where prevention efforts might be focused, as well as the types of serious exposures PCs regularly manage. It is relevant to know whether exposures to these substances are increasing or decreasing. To better understand these relationships, we examined exposures with more serious outcomes per year over the last 13 years for the change over time for each of the 68  dramatic as the decline in use of ipecac, reported use of activated charcoal decreased from 3.7% of pediatric cases in 1993 to just 0.9% in 2013. Table 17A presents the most common 25 substance categories, listed by frequency of human exposure for cases with  Table 17B shows the 25 categories which were increasing most rapidly. Statistical signifi cance of the linear regressions can be verifi ed by noting the 95% confi dence interval on the rate of increase excluding 0 for all, but 3 of the 25 categories. Figure 5 shows the linear regressions for the top 4 increasing categories in Table 17B. Tables 17C and 17D present exposure results for children and adults, respectively, and show the differences between substance categories involved in pediatric and adult exposures. Table 17E reports the 25 categories of substances most frequently involved in pediatric ( Յ 5 years) fatalities in 2013. Table 17F reports the 25 drug ID categories most frequently queried in 2013, highlighting the value of drug ID information to the AAPCC, public health, public safety, and regulatory agencies. Internet-based resources do not afford the caller the option to speak with a health care professional if needed. Proper resources to continue this vital public service are essential, especially since the top 10 substance categories include antibiotics as well as drugs with widespread use and abuse potential such as opioids and benzodiazepines. Table 17G reports the 25 substance categories most frequently reported in exposures involving pregnant patients.

Changes Over Time
Total encounters peaked in 2008 at 4,333,012 calls with 2,491,049 human exposure calls and 1,703,762 information calls. Total encounters decreased 9.3% from 3,373,025 in 2012 to 3,060,122 in 2013. Information calls decreased by 21.4% from 1,025,547 calls in 2012 to 806,347 in 2013, with a 26.8% decrease in drug identifi cation calls and a 8.5 % decrease in HCF information calls. Human exposures decreased by 3.8% from 2,275,141 to 2,188,013 cases.   (1,218) judged to be exposure-related (relative contribution to fatality of 1 -undoubtedly responsible, Figure 4 shows the year-to-year change since 2000 as a percentage of year 2000 for human exposure calls broken down into cases with more serious outcomes (death, major effect, and moderate effect) and less serious outcomes [minor effect, no effect, not followed (non-toxic), not followed (minimal toxicity possible), unable to follow (potentially toxic), and unrelated effect]. Since 2000, cases with more serious outcomes have increased by 4.5% [95% CI (4.0%, 4.9%)] per year from 108,148 cases in 2000 to 171,583 cases in 2013. However, cases with less serious outcomes have consistently decreased since 2008 by 3.7% [95% CI ( Ϫ 4.4%, Ϫ 3.1%)] per year from 2,339,460 in 2008 to 2,015,505 cases in 2013. This decrease in less serious exposures has driven the overall decrease in human exposures since 2008.
Likewise, we see a consistent increase in exposure calls from HCFs ( Figure 3) and for the more severe exposures (Figure 4), despite a decrease in calls involving less severe exposures. Table 19A shows the modest variation in the distribution of suicides and pediatric deaths over the past 2 decades as reported to the NPDS national database. Within the last decade, the percentage of exposures determined to be suspected suicides ranged from 30.3%% to 53.9%, and the percentage of pediatric cases has ranged from 1.5% to 3.2%. The relatively large change seen for 2011 and 2012 refl ects the large increase in indirect death reports in those years. Analyses of suicides and pediatric deaths for direct and indirect reports are shown in Table 19B. Table 20 provides the number of times the specifi c plant was reported to NPDS ( n ϭ 46,376). The 25 most commonly involved plant species and categories account for 39.7% of all plant exposures reported. The top 3 categories in the  (1,218) judged to be exposure-related (relative contribution to fatality of 1 -undoubtedly responsible, 2 -probably responsible, or 3 -contributory).
Deaths are sorted in Table 21 according to the category, substance deemed most likely responsible for the death (Cause Rank), and then patient age. The Cause Rank permits the PC to judge 2 or more substances as indistinguishable in terms of cause, for example, 2 substances which appear equally likely to have caused the death could have Substance Rank of 1, 2 and Cause Rank of 1, 1. Additional agents implicated are listed below the primary agent in the order of their contribution to the fatality.
As shown in Table 5, a single substance was implicated in 89.1% of reported human exposures, and 10.9% of patients were exposed to 2 or more drugs or products. The exposurerelated fatalities involved a single substance in 538 cases (44.2%), 2 substances in 295 cases (24.2%), 3 in 152 cases (12.5%), and 4 or more in the balance of the cases.
In Table 21, the Annual Report ID number [bracketed] indicates that the abstract for that case is included in Appendix C. The letters following the Annual Report ID number indicate: i ϭ Death, Indirect report (occurred in 895, 42.4% of cases), p ϭ prehospital cardiac and/or respiratory arrest (occurred in 462 of 2,113, 21.9% of cases), h ϭ hospital records reviewed (occurred in 497, 23.5% of cases), and        Table 21 percentages is 2,113.   each substance involved in a fatality. The cross-references at the end of each major category section in Table 21 list all cases that identify this substance as other than the primary substance. This alternate name may not agree with the AAPCC generic categories used in the summary tables (including Table 22). Table 18 lists the top 25 minor generic substance categories associated with reported fatalities and the number of single substance exposure fatalities for that category -miscellaneous sedative/hypnotics/antipsychotics, miscellaneous cardiovascular drugs, opioids, and miscellaneous stimulants and street drugs lead this list followed by miscellaneous alcohols, acetaminophen combinations, acetaminophen alone, selective serotonin reuptake inhibitors, and miscellaneous fumes/ gases/vapors. Note that Table 18 is sorted by all substances to which a patient was exposed (i.e., a patient exposed to an opioid may have also been exposed to 1 or more other products) and shows single-substance exposures in the right-hand column.

All fatalities -all ages
The fi rst-ranked substance ( The exposure was acute in 1,183 (56.0%), A/C ϭ acute on chronic in 282 (13.3%), C ϭ chronic exposure in 98 (4.6%), and U ϭ unknown in 550 (26.0%). Table 21 lists each of the 2,113 human fatalities (including death, indirect report) along with all of the substances involved for each case. Please note that the substance listed in column 3 of Table 21 (alternate name) was chosen to be the most specifi c generic name based upon the Micromedex Poisindex product name and generic code selected for that substance. Alternate names are maintained in the NPDS for   Table 8).

Pediatric fatalities -age Յ 5 years
Although children younger than 6 years were involved in the majority of exposures, they comprised 51 of 2,477 (2.1%) of fatalities. These numbers are similar to those reported since 1985 (Table 19A, all RCFs and includes indirect deaths). Table 8 (RCF 1 -3, excludes indirect deaths) shows the percentage fatalities in children Յ 5 years related to total pediatric exposures was 29/1,049,475 ϭ 0.00276%. By comparison, 1,115/833,563 ϭ 0.13% of all adult exposures involved a fatality. Of these 29 pediatric fatalities, 24 the potentially large amount of nicotine in these products (some containing over 100 mg/ml) could potentially produce serious toxicity in both adults and children, if inhaled, swallowed or spilled on the skin. And although fl avored cigarettes have been banned by the FDA since September 2009, there were no restriction on e-cigarette fl avorings. Flavors such as black cherry, caf é mocha, peanut butter cup, and ice cream potentially represent an additional attraction to children. The fi rst exposure to an e-cigarette product was noted in September 2010, with the fi rst child exposure in November 2010. A gradual increase in the number of exposures occurred until the beginning of 2013 when a dramatic increase in the number of exposures to e-cigarettes and their refi lls was seen ( Figure 6). The total number of nonpharmaceutical nicotine exposures has increased, driven primarily by exposures to e-cigarette products. E-cigarette exposure calls peaked in April 2014 and comprised 35% of all nicotine-related single exposure calls. In children, e-cigarettes now account for roughly 25% of exposures, while in other age groups, e-cigarettes exposures have surpassed other tobacco products and account for as many as 65% of exposures. E-cigarette exposures in children under age 5 have serious outcomes in only 1.9% of cases compared with 5.3% in other ages. A decline in exposures has been seen since April 2014, possibly refl ecting increased scrutiny on e-cigarettes and increased state and local regulation. Please note that the data for 2014 are considered preliminary since the 2014 database is not locked.

Discussion
The exposure cases and information requests reported by PCs in 2013 do not refl ect the full extent of PC efforts which also include poison prevention activities and public and health care professional education programs.
NPDS exposure data may be considered as providing " numerator data " , in the absence of a true denominator; that is, we do not know the number of actual exposures that occur in the population. NPDS data include only those exposures which are reported to PCs.
NPDS 2000 -2013 call volume data clearly demonstrate a continuing decrease in total exposure calls. This decline has been apparent and increasing since mid-2007, and refl ects the decreasing use of the PC for less severe exposures. However, in contrast, during this same period, exposures with a more severe outcome (death, major, moderate) and HCF calls have continued a consistent increase. Possible contributors to the declining PC access include declining US birth rates (especially since exposure rates are much higher in children Յ 5 years of age), increasing use of text rather than voice communication, and increased use of and reliance on internet search engines and web resources. To meet our public health goals, PCs will need to understand and meet the public ' s 21st-century communication preferences. We are concerned that failure to respond to these changes may result in a retro-shift with more people seeking medical care for exposures that could have been managed at home by a PC. Likewise, minor exposures may progress to more (2), THC homolog (2), 4-acetoxy-N,N-dimethyltryptamine (2), amphetamine (2), amphetamine (hallucinogenic) (2) and the remainder with1 substance each. The fi rst ranked nonpharmaceutical associated with these fatalities included: cyanide (3), carbon monoxide (2),ethanol (1), methanol (1), freon (1), substance (non-drug) unknown (1), aldicarb (1), and dinitrophenol (1).

Pregnancy and Fatalities
A total of 31deaths of pregnant women have been reported from the years 2000 through 2013. The majority (27 of 31) were intentional exposures (misuse, abuse, or suspected suicide). There was 1 death in pregnant women reported to NPDS in 2013.

AAPCC Surveillance Results
A key component of the NPDS surveillance system is the variety of monitoring tools available to the NPDS user community. In addition to AAPCC national surveillance defi nitions, 35 PCs utilize NPDS as part of their surveillance programs. The Centers for Disease Control and Prevention (CDC), 6 state health departments and 1 state police department run surveillance defi nitions in NPDS. Since Surveillance Anomaly 1, generated at 2:00 pm EDT on 17 September 2006, over 230,000 anomalies have been detected. More than 1,500 were confi rmed as being of public health signifi cance with PCs working collaboratively with their local and state health departments and in some instances the CDC on the public health issues identifi ed.
At the time of this report, 353 surveillance defi nitions run continuously, monitoring case and clinical effects volume and a variety of case-based defi nitions from food poisoning to nerve agents. These defi nitions represent the surveillance work by many PCs, state health departments, the AAPCC, and the Health Studies Branch, Division of Environmental Hazards and Health Effects, National Center for Environmental Health, Centers for Disease Control and Prevention (CDC).
Automated surveillance continues to remain controversial as a viable methodology to detect the index case of a public health event. Uniform evaluation algorithms are not available to determine the optimal methodologies.(9) Less controversial is the benefi t to situational awareness that NPDS can provide.(10) Typical NPDS surveillance data detects a response to an event rather than an event prediction. This aids in situational awareness and resilience during and after a public health event.
A current example of the involvement of the PC system and NPDS can be seen in the following. In January 2010, the AAPCC introduced two generic codes for electronic cigarettes (e-cigarettes): one for the e-cigarette delivery system and one for the liquid nicotine refi lls. As the amount of nicotine in e-cigarettes and their refi lls were not initially regulated by the Food and Drug Administration or any states, they could represent a unique poisoning hazard. As the refi lls were not required to be sold in child resistant containers,  Figure 5. NPDS data mirror CDC data that demonstrates similar fi ndings.(10) Thus, NPDS provides a real-time view of these public health issues without the need for data source extrapolations.
severe morbidity and mortality because of incorrect internet information or no PC management. The net effect could be more severe poisoning outcomes because fewer people took advantage of PC services, with a resultant increased burden on the national health care infrastructure as may be refl ected in the increased number of cases managed in a health care facility this year. The fi gures show the number of calls received per 4-week period by age group for single-substance human poison exposure calls to an e-cigarette device or refi ll ( E-cigarette), traditional tobacco products such as cigarettes, snuff, and chewing tobacco ( Other Tobacco) and the sum of the two groups ( All Nicotine Products) since January 2010. Pharmaceutical nicotine products are excluded (colour version of this fi gure can be found in the online version at www.informahealthcare.com/ctx).

Disclaimer
The American Association of Poison Control Centers (AAPCC; http://www.aapcc.org) maintains the national database of information logged by the country's regional poison centers (PCs) serving all 50 United States, Puerto Rico, and the District of Columbia. Case records in this database are from self-reported calls: they refl ect only information provided when the public or health care professionals report an actual or potential exposure to a substance (e.g., an ingestion, inhalation, or topical exposure), or request information/educational materials. Exposures do not necessarily represent a poisoning or overdose. The AAPCC is not able to completely verify the accuracy of every report made to member centers. Additional exposures may go unreported to PCs and data referenced from the AAPCC should not be construed to represent the complete incidence of national exposures to any substance(s).

Miscellaneous Bites and Envenomations
Other or Unknown Animal Bites                                                                                  Clinical Course: Patient became progressively more hypotensive despite IV fl uid resuscitation, sodium bicarbonate infusion and three vasopressors. ECMO and CRRT were initiated. Metabolic service was consulted for persistent hyperammonemia and initiated a workup for late presenting inborn error of metabolism. Patient was given cobalamin, thiamine, biotin, levocarnitine, and ribofl avin. Toxicology service was then consulted for unresolving metabolic acidosis despite resuscitation and bicarbonate infusion. Patient was given fomepizole. Metabolic acidosis resolved with CRRT. However, the patient ' s cerebral edema worsened, progressing to uncial herniation. Based on the prognosis, the family opted for institution of comfort measures and she expired. Following her death, police investigation revealed that the patient had conducted internet search on methanol poisoning. Multiple empty bottles of windshield wiper fl uid containing methanol were found at the patient ' s home and car. Autopsy Findings: Numerous linear scars on the body were consistent with self-destructive behavior. Other gross and microscopic pathology results were unremarkable. Cause of death was methanol intoxication. Manner of death was suicide.
Case 148. Acute ethylene glycol (antifreeze) per feeding tube: undoubtedly responsible. Scenario/Substances: A 66 y/o male reportedly instilled 100 mL of antifreeze into his GI tract via tube feeding port ∼ 2 h prior to arrival in ED. Past Medical History: Throat cancer, human immunodeficiency virus infection. Laboratory Data: Venous blood gases upon arrival in ED pH 7.42/pCO 2 31/pO 2 35/HCO 3 20/BE -4. Hour 5: Na 147, Cl 107, CO 2 20, Glu 153, BUN 17, Cr 0.7, anion gap 23, Contributory -In the opinion of the CRT, the clinical case evidence establishes that the substances contributed to the death, but did not solely cause the death. That is, the substances alone would not have caused the death, but combined with other factors, were partially responsible for the death. Probably not responsible -In the opinion of the CRT, the clinical case evidence establishes to a reasonable probability, but not conclusively, that the substances associated with the death did not cause the death Clearly not responsible -In the opinion of the CRT, the clinical case evidence establishes beyond a reasonable doubt that the substances did not cause this death. Unknown -In the opinion of the CRT, the clinical case evidence is insuffi cient to impute or refute a causative relationship for the substances in this death.

Selection of Abstracts for Publication
The abstracts included in Appendix C were selected for publication in a three-stage process consisting of qualifying, ranking, and reading. Qualifying was based on the RCF: only RCF ϭ 1 -Undoubtedly Responsible; 2 -Probably Responsible; or 3 -Contributory were eligible for publication. Fatalities by indirect report were excluded beginning with the 2008 annual report. Ranking was based on the number of substances (1/N) and weighted case score. The case weighting factors were the averages chosen based on review team recommendations in 2006. Each case score was multiplied by the respective factors to obtain a weighted publication score: Hospital records * 8.8 ϩ Postmortem * 15.2 ϩ Blood levels * 6.9 ϩ Quality/Completeness * 6.4 ϩ Novelty/Educational value * 13.2. Scores were normalized (z-score) within each reviewer before the fi nal weighting: 25% for Age Z-Score ϩ 25% for Freq Z-Score of 1st cause rank substance ϩ 25% for weighted case scores ϩ 25% for 1/N ϩ 10 for pregnant patient ϩ 10 for patient under 3 years old. The top-ranked abstracts (200 ϩ ties) were each read by individual reviewers (see Appendix A) and the 2 managers (Cantilena and Spyker). Each reader judged each abstract as " publish " or " omit, " and all abstracts receiving 7 or more of 12 publish votes were selected, further edited and cross-reviewed by the two managers.

Abstracts
Abstracts of the cases were selected (see Selection of Abstracts for Publication, above) from the human fatalities judged related to an exposure as reported to US PCs in 2013. A structured format for abstracts was required in the PC preparation of the abstracts and was used in the abstracts presented. Abbreviations, units, and normal ranges omitted from the abstracts are given at the end of this appendix. Case 153. Acute disc battery and acetaminophen ingestion: undoubtedly responsible. Scenario/Substances: A 16 m/o male was brought to the ED after a week of cough. Supratherapeutic doses of acetaminophen may have been given. An X-ray showed a 20-mm coin cell-shaped foreign body in the esophagus. Past Medical History: Previously healthy. Clinical Course: The child was transferred to a tertiary care hospital for endoscopic removal. The battery was successfully removed, and the child was admitted to the ICU. The child developed a massive GI bleed, liver failure, acidosis, and renal failure. He was intubated, sedated, and ventilated; N-acetylcysteine and blood products were administered. The child was taken to the OR where he arrested during exploratory laparotomy. CPR was initially successful, but the child remained hypoxic and hypotensive and died. Autopsy Findings: Not available.
Case 154 . Acute scorpion sting: undoubtedly responsible . Scenario/Substances: A 3 y/o boy awoke at home, crying and complaining of ear pain, and was brought to the ED. Laboratory Data: Initial labs at transferred hospital in PICU, Clinical Course: Patient arrived at ED talking and answering questions, but rapidly developed a grade IV scorpion envenomation with crying, excessive secretions, opsoclonus, writhing, and tachycardia. He was receiving sedatives and analgesia when he developed respiratory distress and arrested. He was intubated and treated with atropine, epinephrine, fl umazenil, bicarbonate. He received fi ve vials of scorpion antivenin post code, was intubated, transferred to a tertiary care hospital, and admitted to the PICU. Lungs were clear and he exhibited posturing. Na 146 Cl, 114, lactate 2.9, AST 221 ALT 81, CK 922, ABG (capillary)-pH 7.48/ pCO 2 26.7/pO 2 61.0/HCO 3 19.9/BE -4.0. Repeat Venous BG-pH 7.29/pCO 2 36/pO 2 49/HCO 3 17/BE -10.0 on FIO 2 45%. CxR " normal. " He was given naloxone to rule out over sedation. Pupils were fi xed and dilated, and no response panting between ventilator breaths. No other medical or genetic abnormalities were found. Patient expired on Day 2 of suspected cerebral edema.
Autopsy Findings: " Complications of probable scorpion sting. " Femoral blood: tryptase 3.6 ng/mL. Case 155 . Acute crotalid envenomation: undoubtedly responsible . Scenario/Substances: A 53 y/o 57 kg male was bitten while attempting to cut the rattle off a rattlesnake, which he presumed was dead. He developed an anaphylactic reaction with cardiopulmonary arrest. He was unresponsive to CPR measures including cardioversion, was intubated, and ventilated. Physical Exam: After resuscitation HR 110, BP 94/50, he had an edematous right hand with three puncture marks. Clinical Course: He was given dopamine, 6 vials of antivenin (Fab fragment), tetanus toxoid, epinephrine, methylprednisolone, and diphenhydramine. He was transferred to a tertiary care hospital and admitted to the ICU 3 h post exposure. He was ventilated with FiO 2 100% ϩ PEEP 5 with no pupil response. Bite site slightly swollen with no apparent progression. At 20 h post bite (14 vials of antivenin) he remained on the ventilator, receiving norepinephrine IV. Pupils were pinpoint and nonreactive. The affected hand measured 19.5 cm, was ecchymotic and blistering. By 24 h post bite (26 vials antivenin), HR 123 and BP 115/63, a femoral catheter was placed and dialysis started for acute kidney injury. On Day 3 (34 vials of antivenin), there were no neurological changes. On Day 4, his entire body was mottled, and he was purple from his nipple line up. The affected arm was ecchymotic and blistered up to his bicep. Right pupil was 3 mm and left pupil 4 mm and non-reactive. EEG showed "severe brain damage", gag refl ex was absent, and he had negative dolls eye refl ex. He was receiving multiple vasopressors and IV NS. On Day 5, based on the prognosis, the family opted for institution of comfort measures and he expired later that day. Autopsy Findings: Not performed.
Case 161. Acute cyanide exposure: undoubtedly responsible. Scenario/Substances: A 19 y/o male purchased several grams of NaCN and KCN salts online, collapsed at home, EMS intubated, and was transported to the ED. Past Medical History: Asperger ' s syndrome, depression, previous suicide attempt with chloroform. anion gap 25, INR 1.48, lactate 20, serum acetaminophen and salicylate not detected, lithium 0.2 mmol/L, digoxin 0.2 ng/mL, UDS negative. Serum CN ∼ 10 mg/L (potentially toxic Ͼ 0.5 mg/L), 1.3 mg/L (thought drawn after fi rst dose of hydroxocobalamin). Clinical Course: On arrival in the ED, he was unresponsive, GCS 3, pupils midrange and fi xed. He was reintubated, remained profoundly tachycardic and hypotensive despite maximum doses of norepinephrine and dopamine. Further history from family disclosed that patient ' s access to cyanide salts. Initial labs were notable for profound metabolic acidosis with markedly elevated lactate. ECG showed nonspecifi c intra ventricular conduction delay with QRS 120 which was improved to 94 -100 after sodium bicarbonate. He received hydroxocobalamin 5g x3 doses total, with repeat BP improved from systolic 40 to 60 to 70-80 then to 180 -200 after third dose. HR increased to 180s after 3rd dose of hydroxocobalamin. Repeat labs showed slight improvement in acidosis and lactate; however hypotension recurred requiring a 4th dose of hydroxocobalamin with minimal improvement. Head CT showed diffuse subarachnoid hemorrhage, poorly differentiated gray-white matter with global effacement consistent with anoxic encephalopathy, and hypoxic ischemic injury. Based on the prognosis, the family opted for institution of comfort measures and he expired on Day 1. Autopsy Findings: External exam and laboratory evaluation performed only due to family ' s religious wishes. Lumbar tap with bloody CSF with RBCs settling and residual maroon CSF. Ante mortem blood prior to hydroxocobalamin treatment screened positive for CN ( ∼ 10 mcg/mL, reporting limit 0.3 mcg/mL). Cause of death: hypoxic encephalopathy and possible subarachnoid hemorrhage complicating acute cyanide toxicity. The manner of death was suicide.
Case 171. Acute ammonia inhalation and ocular: contributory . Scenario/Substances: A 45 y/o male was driving a semitruck carrying anhydrous ammonia that collided with a train. There was no damage to the cab and he was alert, but soon experienced diffi culty breathing. EMS found him in respiratory distress with confusion, intubated him, noted vocal cord edema, and transported him to the ED. Physical Exam: In the ED, bilateral scleral and conjunctival injection, erythematous eyelids, pupils equal and reactive to light, moist oral mucosa, diminished lung sounds in right base with occasional expiratory wheezes, extremities: 1 -2 ϩ edema of right lower extremity with trace lower extremity edema on the left. BP 135/63, O 2 sat 98% on 100% FiO 2 , T 36 ° C.
Laboratory Data: ABG-pH 6.91/pCO 2 38/pO 2 153/HCO 3 7/BE 26, WBC 20. 5,Hgb 20.4,Hct 63.4,platelets 314 Laboratory Data: ABG-pH7.11 / pCO 2 82 / pO 2 299 / HCO 3 26.5, WBC 22.3, CO 2 19.6 Clinical Course: He was admitted to the ICU, eyes copiously irrigated, and ophthalmology examination completed. He was maintained on mechanical ventilation, and CxR showed bibasilar infi ltrates; he received prophylactic antibiotics for presumed aspiration pneumonia. Respiratory status improved, and he was weaned from ventilator on the morning of Day 5. Later on that day, he developed increasing dyspnea, bradycardia with a decline in O 2 sats that were unresponsive to supplemental O 2. A code was called, the patient re-intubated, but had ventilator asynchrony and was diffi cult to ventilate. He became tachycardic, was on maximal IV propofol and midazolam when he had a pulmonary embolism and was suspected despite prophylactic heparin administration. Prior to obtaining a CT of the chest, he had a bradycardic episode, unresponsive to atropine, which quickly became a PEA arrest. He underwent ACLS resuscitation for 40 minutes without return of circulation. He expired on Day 6. Autopsy Findings: Not performed per family.
Case 185. Acute cyanide ingestion: undoubtedly responsible . Scenario/Substances: A 73 y/o male jeweler presented to the ED with his wife via private vehicle. Past Medical History: CAD, s/p CABG and pacemaker placement. Laboratory Data: ABG-pH 7.32 / pCO 2 18 / pO 2 453 / HCO 3 17 / BE 8, Na 148, K 3.8, Cl 115, CO 2 17, anion gap 16, BUN 23, Glu 94 ALT 19, AST 75, serum ethanol not detected. Clinical Course: Patient was acting normally in the ED waiting room. The patient's wife reported that he left the waiting room, telling her that he was going to get some apple juice. Upon return, he sat down and slumped over in his chair. ED staff found the patient to be apneic and pulseless and began resuscitation. He was taken to a room where standard resuscitative measures were instituted, including IV access, chest compressions, endotracheal intubation, placement on a ventilator and provision of oxygen. Initial rhythm on the monitor was VT. Return of spontaneous circulation was established. He was tremulous, unresponsive, "posturing", skin clean and dry, gag refl ex and corneal refl exes absent, pupils 5 -6 mm and nonreactive A dopamine infusion was started. Inspection of his person revealed a small vial of potassium cyanide in his pocket and a suicide note around his neck stating he wanted "no code." Further history at that time revealed that he was in need of another "cardiac surgery" and was "just done with it." The patient received sodium nitrite and sodium thiosulfate in standard doses. Computed tomography of the brain revealed "global infarcts" and "subarachnoid hemorrhage". The patient was admitted to the ICU where he was declared that his brain was dead the next day, and life support was withdrawn. Autopsy Findings: Autopsy included hemorrhagic gastritis, marked cerebral edema, cerebellar tonsillar herniation Na 147 Cl 110 BUN 17 Glu 135 K 4.5 CO 2 12 Cr 1.2 and infarct, cerebral venous sinus thrombosis. Postmortem specimens of heart blood were negative for amphetamines, barbiturates, carisoprodol, cocaine, opiates, and THC metabolite. Hospital blood lidocaine was Ͼ 1, 000 mg/mL, believed secondary to use lidocaine during ACLS resuscitation. Premortem blood from the hospital was positive for cyanide (qualitative). Urine specimen and postmortem blood specimens were negative for cyanide. Cause of death: cyanide intoxication. Manner of death: suicide.
Case 186. Acute potassium aluminum sulfate parenteral: undoubtedly responsible. Scenario/Substances: A 78 y/o 88 kg male received 10 g potassium aluminum sulphate in 1 L D5W IV instead of per urethral catheter. He received 600 ml of the solution IV in 3 -4 h after which patient felt cold and became tachycardic and dyspneic. Past Medical History: Hematuria, prostate cancer. Physical Exam: BP 132/82, HR 114, RR 18, T 97.3F, Urine cherry in color, urine output total volume 600 ml. Laboratory Data: ABG-pH 7.54 / pCO 2 30 / pO 2 359, O 2 sat 100% on ventilator. Na 136, K 4.0, BUN 9-17, Cr 0.89-1.26, Hgb 10.1, Hct 28, platelets 222, INR 2.2-2.8. Clinical Course: CxR showed pulmonary embolism. He was twice successfully resuscitated following cardiac arrest. He intubated and sedated in the ICU, completed fi rst dose of IV deferoxamine 1g in 1 L at 15 mg/kg/hr and hemodialysis. He received a second dialysis and deferoxamine treatment on Day 2. Attempts were made to wean patient off sedation on Day 3, but he became agitated and sedation was restarted. His BP became labile and norepinephrine was started. He was found to have blood clots in his urinary catheter. Based on the prognosis, the family opted for institution of comfort measures and he expired on Day 3 Autopsy Findings: Not available Case 199. Acute hypochlorite parenteral: probably responsible. Scenario/Substances: This 63 y/o male had just completed a hemodialysis run on his home dialysis machine. He forgot to disconnect himself from the machine before putting bleach into the machine to clean it and infused ∼ 60 ml of sodium hypochlorite bleach into his dialysis catheter. He " felt funny " and called EMS. He had a cardiac and respiratory arrest during transport, CPR was begun, intubation was attempted, and he was transported to the ED. He received multiple rounds of epinephrine and atropine enroute to the ED. Past Medical History: Multiple surgical procedures, including right and left nephrectomies, partial ureterectomy, adrenalectomy, parathyroidectomy, arteriovenous fi stula, autogenous arteriovenous fi stula, and insertion of a tunneled centrally inserted central venous catheter. He had seasonal allergies, smoked cigarettes daily, used alcohol 1 -2 times a month. Physical Exam: The patient was unresponsive. His skin was cool. No detectable BP or HR.
Case 206. Acute laundry detergent (pod) ingestion: undoubtedly responsible. Scenario/Substances: A 7 m/o male bit into a laundry detergent pod and the contents entered his mouth. The child was crying with occasional cough and became somnolent. EMS was notifi ed and transported the child. Vomiting occurred en route to the ED. Past Medical History: Recent upper respiratory tract and urinary tract infections treated with cefdinir, but did not complete the course because of runny red stools. Physical Exam: Somnolent with upper airway wheezing and retractions; moderate respiratory distress. HR 170, RR 30, T 37 ° C, O 2 sats in the 80s% on RA and improved with supplemental oxygen. His palate and pharyngeal cavity had visible red spots. Laboratory Data: ABG-pH 6.50 / pCO 2 70.5 / pO 2 27, Na 156, K 2.8, Cl 126. CxR right upper lobe infi ltrate. Clinical Course: During transfer preparations in the ED, the patient experienced a seizure. He was more lethargic with agonal breathing in the 50 ' s. An interosseus catheter was placed, and he was endotracheally intubated; 3 h after exposure, the patient experienced a cardiac arrest and could not be resuscitated. Autopsy Findings: Mild hyperemia of the oropharynx and tracheal without evident burns or ulcerations. There was a small amount green brown gastric content. There was signifi cant asymmetric pulmonary congestion on right and some cerebral edema. UDS was negative. Central postmortem blood propylene glycol of 33 mg/dl; gastric contents: propylene glycol of 370 mg/dL. No ethylene or diethylene glycol detected. The death was determined to be accidental exposure to laundry soap detergent.
Case 209. Acute magnets and carbaryl ingestion: undoubtedly responsible . Scenario/Substances: A 19 m/o female was examined in the ED for complaints of vomiting and diarrhea, instructions for supportive care were given, and the patient was released. The next day she was found unresponsive by her mother. EMS and police were called, bystander CPR was performed and she was transported to the ED. Past Medical History: Good general health Clinical Course: On arrival to the ED, the patient had expired, but PALS was performed. Blood was noted in the nose and mouth, but no other signs of trauma were noted. ABG-pH 6.50/pCO 2 46/pO 2 36, Na 155, K 6.2, Glu 20 Hgb 3.6. Skeletal survey to rule out abuse was performed post-mortem in the ED did not reveal any acute or healing fractures. Portal venous gas and pneumatosis intestinalis was noted. Seven small metallic spherical radio dense foreign bodies were present within the posterior medial aspect of the left abdomen in a linear fashion. EMS and police reported that the child ' s room was covered in a while powder. The mother stated that the powder was carbaryl insecticide, which had been placed in the room at an unknown time. Autopsy Findings: Cause of death was listed as ischemic bowel due to spherical magnets found in the small intestine, causing pressure necrosis when the magnets presumably adhered to one another with a portion of small bowel between them. Other conditions related to the death were bed sharing and unsafe sleep surface. No evidence of serious trauma was noted externally. Internal examination revealed the seven above-mentioned magnets to be within the bowel in a linear formation. The stomach and esophagus were normal, while the small bowel proximal to the magnets was hyperemic. Small bowel distal to the magnets was normal in appearance. Femoral blood was drawn and analyzed. Carbaryl was NOT detected in blood. Ketamine was detected at 7.0 mcg/ mL, but this was administered in the ED during intubation. Nor-ketamine was not detected. Heart blood was negative for ethanol. Vitreous electrolytes: Na, 140; K, 18; Cl, 131; Ca, 1.6; Mg, 0.92; Glu, 78; lactate, 21 mmol/L; urea nitrogen, 10; Cr 0.8. Powder samples ϫ 3 were assessed: all 3 samples were positive for carbaryl and 1-naphthalenol.
Case 224 . Acute carbon monoxide inhalation: undoubtedly responsible. Scenario/Substances: An 11 y/o male was found dead in bed in pool of emesis in a hotel room. His mother was found on the bathroom fl oor, unconscious suffering from severe CO toxicity. The source was determined to be a retrofi tted swimming pool heater that vented very close to the window with a faulty exhaust line that leaked into the room as well. Very high levels of CO were noted when the pool heater was turned on later. Two deaths occurred in the same hotel room 2 months earlier, initially attributed to " heart attacks " , but were later determined to be due to carbon monoxide. Laboratory Data: Postmortem COHb level from aortic blood was reported as Ͼ 60%. Autopsy Findings: Autopsy demonstrated pulmonary edema and congestion. Petechiae were distributed over head and neck. Cause of death was carbon monoxide toxicity, with the manner being accidental.
Case 283. Acute hydrogen sulfi de inhalation: undoubtedly responsible. Scenario/Substances: A 53 y/o male collapsed inside an asphalt truck container and was pulled out by his son. His son also experienced symptoms. The tank was believed to contain hydrogen sulfi de. EMS found that the patient had agonal breathing, intubated him with a laryngeal tube, and removed his clothing prior to transport to the ED. Past Medical History: Hypertension. Physical Exam: Upon arrival to the ED, the patient was unconscious with seizure-like movements. The laryngeal tube was exchanged for endotracheal intubation during which a large amount of emesis occurred resulting in aspiration. He was given hydroxocobalamin. On arrival, BP 130/80, HR 87, and O 2 sat 82% on 100% FiO 2 . The urine was found to be in deep purple after the hydroxocobalamin treatment. Laboratory Data: Initial ABG-pH 7.07 / pCO 2 58.0 / pO 2 60 / HCO 3 10.0, K 3.4, Cl 108, CO 2 18, BUN 16, Cr 1.4, Glu 146, Ca 8.1, AST 108, ALT 65. CK 807, INR 1.1, troponin I 0.5, and methemoglobin 0.8%. Clinical Course: The patient was sedated using propofol, midazolam and fentanyl, and mechanically ventilated. He was given IV fl uids and antibiotics. On hour 12, the patient became hypotensive, tachycardic, developed ECG changes consistent with an anterior wall myocardial infarction, and developed a PEA arrest. He was resuscitated with CPR and epinephrine, sodium bicarbonate, and calcium gluconate. He required post-arrest epinephrine and norepinephrine infusions. Post-arrest: pH 7.11, lactate 14.7, troponin I 3.5. He developed a T 38.7 ° C. The patient had a second cardiac arrest at Hour 21 and could not be resuscitated. Autopsy Findings: Left ventricular hypertrophy and nephrosclerosis. No drug or chemical levels detected. The death was determined to be from an accidental exposure to hydrogen sulfi de.
Case 316 . Acute carbon monoxide inhalation: undoubtedly responsible. Scenario/Substances: A 72-year-old female was found unresponsive and on respiratory arrest in her hotel room bed by housekeeping. CPR was initiated. She was intubated and taken to the local ED. Resuscitation attempts were unsuccessful and she expired. Her husband was found dead in the bathtub. The hotel room was not assessed for the presence of any gases. Past Medical History: hypertension and atrial fi brillation. Autopsy Findings: The ME initially assumed the patient and her husband died of overdoses. An autopsy showed pulmonary edema and mild cardiomegaly. Toxicology revealed a COHb of Ͼ 60%. Results were fi nalized 6 weeks after the deaths, and 1 week prior to an 11-year-old male dying of carbon monoxide toxicity in the same hotel room. An investigation determined the heater for the hotel ' s indoor pool was below the hotel room where all 3 deaths occurred and the heater exhaust was not functioning properly.
Case 318. Acute carbon monoxide inhalation: undoubtedly responsible. Scenario/Substances: A 73-year-old male was found dead in the bathtub of his hotel room by housekeeping. CPR was initiated, but he was pronounced dead at the scene. His wife was found unresponsive in the bed. The hotel room was not assessed for the presence of any gases. Autopsy Findings: Pulmonary edema, severe atherosclerosis, and cardiomegaly. The ME initially assumed that the Copyright © Informa Healthcare USA, Inc. 2014 AAPCC 2013 Annual Report of the NPDS 1267 Bilirubin 0.8, AST 35, ALT 23, Alk phos 41, blood lead Ͼ 160 mcg/dL. Clinical Course: The patient was sedated, placed on high dose antiepileptic agents and started on dimercaprol followed by Ca disodium EDTA. Despite maximal therapy, the patient remained in status epilepticus, and was treated with phenytoin, levetiracetam, propofol, midazolam, and phenobarbital. He continued to have subtle twitching during the hospitalization and seizure activity on his EEG. Repeat blood lead: 95 mcg/dL at 48 h after the initiation of chelation and 60 mcg/dL at 96 h. Despite continued therapy, the patient made no neurologic recovery. When propofol sedation was reduced, the patient would again start to seize. On Day 7, he became hemodynamically unstable with hypotension and bradycardia. Based on the prognosis, the family opted for institution of comfort measures and he expired on Day 9. Autopsy Findings: Not available.
Case 355. Chronic freon inhalation: undoubtedly responsible. Scenario/Substances: A 33 y/o male was huffi ng compressed Freon in the woods throughout the day with frequent loss of consciousness. He was found passed out in the woods and brought to the ED by EMS. Past Medical History: Chronic back pain, reconstructive surgery following a motor vehicle accident, anxiety and depression. History of huffi ng including a case of patient and his wife died of overdoses. Toxicology revealed a COHb of Ͼ 60%. Results were fi nalized 6 weeks after the death, and 1 week prior to an 11-year-old dying of carbon monoxide toxicity in the same hotel room. An investigation determined the heater for the hotel ' s indoor pool was below the hotel room where all 3 deaths occurred and the heater exhaust was not functioning properly.
Case 342. Lead and ethanol ingestion: undoubtedly responsible. Scenario/Substances: A 73 y/o male made and drank his own moonshine, and developed altered mental status the evening before presentation, and began having seizures at home. EMS intubated him, gave several doses of benzodiazepines, and transported him to the ED. Past Medical History: His wife had been recently hospitalized and intubated secondary to lead encephalopathy thought to be caused by drinking homemade moonshine. She recovered with chelation to near baseline. She and the entire family were counseled to discontinue the use of this moonshine. Physical Exam: In the ED, he was in status epilepticus, intubated, sedated. He was afebrile, BP 127/98, HR 80. Laboratory Data: ABG-pH 7.36 / pCO 2 33 / pO 2 153 / HCO 3 19, pneumonitis 1 year earlier resulting from chronic huffi ng of compressed air. Laboratory Data: Na 137, Cl 97, CO 2 17, anion gap 23, BUN 23, Cr 1.5, Glu 220, AST 53, CK 1,000, troponin 0.24, Ca 5.1, Ca (ionized) 0.6, WBC 20. Clinical Course: On ED arrival, the patient was agitated, HR in the 140s. He was dehydrated but afebrile. He was given IV fl uids, lorazepam, and promethazine. Within 2 h of arrival in the ED, he lost consciousness and began to seize. He developed VT and was electrically cardioverted to a sinus rhythm with HR 110. Calcium was administered. Labs showed albumin 3.8, ALT 22, Mg 1.0, CKMB 20.9, and Phos 1.7. Repeat Ca 5.3, repeat CK 2,245. The patient had another seizure ∼ 3 h later and developed VF, received defi brillation twice, was then intubated and transferred to the ICU. At that time he remained tachycardic, HR 106, BP 96/69, RR 20. Propofol infusion was started and he received electrolyte replacement. The patient expired ∼ 9 h post ED arrival. Autopsy Findings: No autopsy was performed. Coroner concluded the death was due to fatal cardiac arrhythmias as a result of prolonged huffi ng of fl uorinated hydrocarbons.
Case 367. Acute lamp oil ingestion/aspiration: probably responsible. Scenario/Substances: A 15 m/o 12-kg male ingested/ aspirated torch fuel at home. EMS transported the patient to the ED. Clinical Course: In the ED, the patient required oral intubation, was placed on oscillator ventilation, and arrangements were made for transfer for ECMO. Initial BP was " unstable " , pH 6.8, " CO 2 in the 100 ' s " , ABG-pH 7.183 / pO 2 64 / CO 2 57.9 / HCO 3 21.3 / BE 7. His status deteriorated during transfer to the tertiary care hospital. On arrival in the PICU, O 2 sats 50 -60%, O 2 sat100% after ECMO. BP 94/42, HR " 140 ' s " , T 37.6 ° C. EEG showed no activity. After aggressive treatment over a course of 4 days, an EEG was done and showed no activity. Brain death was declared Day 4. Autopsy Findings: Not available .
Case 368. Acute gasoline ingestion/aspiration: undoubtedly responsible . Scenario/Substances: A 17-month-old male ingested gasoline, choked, vomited, and rapidly developed severe respiratory distress. EMS found him coughing, tachypnea and dyspneic and transported him to the ED. Supplemental oxygen was provided in ambulance, O 2 sat 90%, but the child deteriorated and required intubation by EMS en route. Laboratory Data: CxR showed " white-out " of lungs. Clinical Course: In the ED O 2 sat fell to 70%, and PEEP was added; he was transferred by air to a tertiary care hospital where he suffered a bradycardic arrest ∼ 7 h after ingestion initially responsive to atropine, epinephrine, and sodium bicarbonate. He arrested again a short time later and could not be resuscitated. Clinical Course: Patient was placed on a hypothermia protocol, given NS 2 L bolus and admitted to the ICU where a norepinephrine infusion was started. Over the following 48 h hypothermia and tachycardia resolved and BP was stabilized with pressors but patient remained completely unresponsive. Cerebral fl ow study demonstrated no fl ow, EEG demonstrated diffuse background with little appreciable brain activity, and non-contrast brain MRI showed cerebral edema, transtentorial and tonsillar herniations. On Day 3, the patient was declared brain dead. Autopsy Findings: Not performed.
Case 389. Acute malathion ingestion: undoubtedly responsible. Scenario/Substances: A 49 y/o man intentionally drank a bottle of malathion. EMS was called and transported the patient to the ED.
Case 369. Acute hydrofl uoric acid ingestion: undoubtedly responsible . Scenario/Substances: A 2 y/o male presented to the ED 30 min after ingesting a mouthful of automotive wheel cleaner. The substance had been stored in a water bottle, and was given to him by his grandmother, who thought she was giving the child a bottle of water. Physical Exam: He presented awake and alert, but was drooling. Laboratory Data: Initial laboratory work included a Ca, 8.1; K, 3.0; and venous pH, 7.21. Several h later Ca 2.6. Clinical Course: Initial treatment consisted of IV calcium gluconate. Approximately 3 h after ED arrival, the patient had a cardiac arrest. He was resuscitated and given additional calcium. He was transferred to a tertiary children ' s hospital where he was aggressively treated with IV calcium, and suffered a terminal cardiac arrest ∼ 7 h after ingestion. Autopsy Findings: Not performed.
Case 377. Acute dinitrophenol ingestion: undoubtedly responsible. Scenario/Substances: A 19 y/o male purchased dinitrophenol on the internet as a weight loss supplement, took 1 dose (quantity unknown) in the morning, and began feeling unwell late that day and sought care at the ED. Past Medical History: No reported serious, chronic medical problems. No psychiatric history. Laboratory Data: ABG-pH 7.46, Cr 1.4, Phos 6, other electrolytes unremarkable, lactate 2.9 mmol/L, salicylates 27, serum acetaminophen and ethanol not detected. Clinical Course: Upon arrival to the ED, the patient was awake and conversant, HR 120 -140, and hypertensive. He was given IV fl uids and lorazepam. Mental status declined over the following 2 h, HR increased to 170s, systolic BP 100, T 38.1 ° C, RR 45, and O 2 sat 99% on room air. He received additional IV fl uids and IV lorazepam. Methemoglobin was not detected: respiratory and mental status continued to worsen requiring intubation and external cooling measures which were initiated. The patient suffered an asystolic cardiac arrest, ACLS was initiated, but resuscitation was unsuccessful. During the resuscitation T was Ͼ 42.71 ° C (the upper limit on the thermometer). Autopsy Findings: not available.
Case 380. Acute-on-chronic dinitrophenol and diphenhydramine ingestion: probably responsible. Scenario/Substances: A 28 y/o male was using dinitrophenol 200 mg a day for weight loss, ingested 4 g in a suicide attempt. Past Medical History: Obesity Physical Exam: Awake but "groggy" and diaphoretic on presentation, BP 156/74, HR 174, T 37.9 ° C, RR 40. Laboratory Data: None provided Clinical Course: The patient was given lorazepam IV for agitation. Due to the expected high lethality of DNP, lipid emulsion infusion was given. Prior to transfer to a transferred to a tertiary care hospital, HR 184, BP 163/62, and T 38.4 ° C.
The patient was extremely agitated during transport and 7 hospital personal were required to manage him. He had a cardiac arrest soon after arrival at the tertiary care hospital from which he could not be resuscitated. Autopsy Findings: Post mortem blood was negative for cocaine, amphetamines, THC and toxic alcohols. 2, 4-dinitrophenol was not detected (specifi c HP-TLC assay). Trace amounts of diphenhydramine (within the therapeutic concentration) were found. ME fi nal diagnosis: death probably due to 2, 4-dinitrophenol toxicity.
Case 384 . Acute DEET (insect repellent) ingestion: undoubtedly responsible . Scenario/Substances: A 37 y/o male obtained and ingested a 6 ounce bottle of DEET insect repellant. Patient had a witnessed seizure and EMS was summoned. Patient had a VT cardiac arrest enroute to hospital. He received 20 min of CPR and received epinephrine, sodium bicarbonate, dextrose, naloxone and atropine with return of spontaneous circulation. He was intubated and given oxygen prior to arrival at the ED. Past Medical History: Developmental delay (profound, lived in a group home), PICA, and cardiomegaly. Physical Exam: BP 84/60, HR 96, RR 18, O 2 sat 100% on 100% FiO 2 , T33.5 ° C. Head atraumatic, pupils fi xed and dilated at 8 mm, oroendotracheal tube in place, multiple abrasions on anterior chest with some oozing of blood, no bowel sounds, and urinary catheter in place with grossly bloody urine without clots. Laboratory Data: ABG-pH 7.15/pCO 2 42.1/pO 2 172/HCO 3 13.9, lactate 9.1, PT 22.9, INR 2, AST 404, ALT 397 had a junctional bradycardia with escape rhythm, and his ECG showed a new LBBB. He was treated with CVVH and a bicarbonate drip. He was given antibiotics for possible sepsis. He also received fi lgrastim for his leukopenia. His lactate level peaked at 27.9 mmol/L. He developed hepatic failure with peak AST 3,495, ALT 1,676, bilirubin 7.1, CK rose to 3,500. He died from multi-organ failure 24 h after admission. Autopsy Findings: The ME reported colchicine 4.0 ng/mL from premortem hospital blood (1 hour after arrival in the ED).
Case 1085. Acute salicylate ingestion: undoubtedly responsible. Scenario: An 11 m/o male was given a medicine bottle to play with by his parents and was later found with the open bottle of enteric coated 325 mg salicylic acid. The patient had orange residue on his face, 1 intact tablet was removed from his mouth by a family member, and he was brought to the ED. Laboratory Findings: The 6-hour salicylate level was 107 mg/dL and would later peak at 123 mg/dl. Na 146, K 2.6, anion gap 29, Glu 712, BUN 13, Cr 1.2. Clinical Course: In the ED, the patient was alert and age appropriate. HR 154, RR 30, T 37 ° C, O 2 sat 100% on room air. Family initially reported that, at most, 7 tablets were unaccounted for. He vomited thrice with 2 aspirin tablets visible in the emesis. He was given activated charcoal, IV fl uids, and sodium bicarbonate 40 meq/hr. He was admitted to the PICU where he became severely tachycardic (HR 221), tachypneic (RR 45) and hyperthermic (T 38.5 ° C). He experienced electrolyte abnormalities including hypokalemia, hypernatremia, and hyperglycemia. On Day 2, the patient was intubated in preparation for transfer to a HCF that could provide hemodialysis when he went into cardiac arrest and expired. Autopsy Findings: Petechial hemorrhages of the heart, thymus, and brain. The brain had non-volumetric subdural and subarachnoid hemorrhages. The salicylate concentration of antemortem blood 7 h post ingestion was 850 mg/L (85 mg/dL). The manner and cause of death was accidental ingestion resulting in salicylate toxicity.
Case 1088. Acute methadone ingestion: undoubtedly responsible. Scenario/Substances: Aunt of a 19 m/o female was watching the child while mom attended a recovery group meeting. When mom arrived home she noticed the child was tired, so she put her down for a nap. When mom went to wake child, she noticed her lips were blue so she took her to the ED. Laboratory Data: UDS positive for methadone. Clinical Course: Upon arrival to ED, child ' s skin was ashen and oxygen was given. UDS came back positive to methadone, naloxone was given, her color improved, and she became more alert. Continuous naloxone infusion was started at 25 mcg/kg/min. She was protecting her own airway. The next day, child developed respiratory depression, apnea, and her HR dropped to 80 ' s. She was intubated using rapid sequence intubation with fentanyl, her HR improved, and naloxone infusion was continued. That evening, she went into acute respiratory failure and suffered a cerebral herniation. Emergency craniotomy was performed and drain inserted, but pressures in her brain remained high. Epinephrine, norepinephrine, and vasopressin were used for pressure support. She developed diabetes insipidus. Continuous EEG showed no activity. She was determined to be brain dead, and the organs were donated. Autopsy Findings: Acute necrosis of brain tissue related to methadone toxicity. Pre-mortem: methadone 248 ng/mL, EDDP 13 ng/mL. Case 1096. Acute sevofl urane inhalation: undoubtedly responsible. Scenario/Substances: A 37 y/o male nurse anesthetist was found at home hooked up to an anesthesia machine with sevofl urane. Patient was found in cardiopulmonary arrest, was resuscitated, and intubated. Initial post-resuscitation rhythm was atrial fl utter with rapid ventricular response. He had seizure-like activity and was given phenytoin Past Medical History: Insomnia (reported to be using his anesthesia machine for sleep) Laboratory Data: Initial Ca (ionized) 1.02. Toxicology screen for drugs of abuse and toxic alcohols was negative. Clinical Course: He received Ca IV for low Ca, a calcium channel blocker IV for his atrial fl utter, and was placed on 48 h post-resuscitation hypothermia protocol. BP 101/58, HR 89, O 2 sat 100 % on O 2 , T 32 ° C. Head CT was consistent with anoxic brain injury. He remained paralyzed with cis-atracurium, received propofol for seizure and sedation, and was receiving norepinephrine for pressure support. After 2 EEGs, he was declared brain dead and his organs were made available for donation. Autopsy Findings: Sevofl urane from blood drawn at admission 5.9 mcg/mL (upper reporting limit is 0.10 mcg/mL). Post mortem phenytoin 12 mcg/mL. No other injuries or pathology were found on autopsy.
Case 1100. Acute lidocaine parenteral: undoubtedly responsible. Scenario/Substances: A 77 y/o female nursing home resident came to the ED for an unknown reason. Past Medical History: COPD, hypertension, diabetes mellitus, seizure disorder, and s/p pacemaker placement. Laboratory Data: K of 6.0 was reported, but ECG did not show signs of hyperkalemia. Clinical Course: The patient was to receive 25 g dextrose and 10 U insulin for the hyperkalemia, instead she received an unknown amount (40 -100 mg) of lidocaine IV. Immediately after the bolus, she became unresponsive, possibly had a seizure, developed a wide complex bradycardia that her pacemaker did not capture, and BP 130 ' s/80 ' s. She received dextrose, Ca, and sodium bicarbonate to treat her hyperkalemia. She developed asystole during the next 30 min. ACLS was initiated, and the patient was given lipid emulsion, but she could not be resuscitated.