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NPDS Report 2011

2011 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 29th Annual Report

Pages 911-1164 | Published online: 31 Dec 2012

Abstract

Background: This is the 29th Annual Report of the American Association of Poison Control Centers’ (AAPCC) National Poison Data System (NPDS). As of 1 July 2011, 57 of the nation's poison centers (PCs) uploaded case data automatically to NPDS. The upload interval was 8.43 [6.29, 13.7] (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 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 2011, 3,624,063 closed encounters were logged by NPDS: 2,334,004 human exposures, 80,266 animal exposures, 1,203,282 information calls, 6,243 human confirmed nonexposures, and 268 animal confirmed nonexposures. Total encounters showed an 8.3% decline from 2010, while health care facility exposure calls increased by 4.8%. Human exposures with less serious outcomes decreased by 3.4% while those with more serious outcomes (moderate, major or death) increased by 6.8%. All information calls decreased by 17.9% and health care facility (HCF) information calls decreased by 2.9%, Medication identification requests (Drug ID) decreased by 24.1%, and human exposures reported to US poison centers decreased by 2.2%.

The top 5 substance classes most frequently involved in all human exposures were analgesics (11.7%), cosmetics/personal care products (8.0%), household cleaning substances (7.0%), sedatives/hypnotics/antipsychotics (6.1%), and foreign bodies/toys/miscellaneous (4.1%). Analgesic exposures as a class increased most rapidly (10,134 calls/year) over the last 11 years. The top 5 most common exposures in children aged 5 years or less were cosmetics/personal care products (14.0%), analgesics (9.9%), household cleaning substances (9.2%), foreign bodies/toys/miscellaneous (6.9%), and topical preparations (6.6%). Drug identification requests comprised 59.5% of all information calls. NPDS documented 2,765 human exposures resulting in death with 1,995 human fatalities judged related (RCF of 1-Undoubtedly responsible, 2-Probably responsible, or 3-Contributory).

Conclusions: These data support the continued value of poison center 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 US. 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.

View correction statement:
2011 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 29th Annual Report

WARNING:

Comparison of exposure or outcome data from previous AAPCC Annual Reports is problematic. In particular, the identification of fatalities (attribution of a death to the exposure) differed from pre-2006 Annual Reports (see Fatality Case Review – Methods). Poison center death cases are described as all cases resulting in death and those determined to be exposure-related fatalities. Likewise, and (Exposure Cases by Generic Category) since year 2006 restricts the breakdown including deaths to single-substance cases to improve precision and avoid misinterpretation.

Introduction

This is the 29th Annual Report of the American Association of Poison Control Centers’ (AAPCC; http://www.aapcc.org) National Poison Data System (NPDS).Citation1 On 1 January 2011, fifty-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 poison centers. Poison Centers (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 all, 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 regional PCs is manifest as the number of exposure and information call encounters exceeds 3.6 million annually. PC encounters either involve an exposed human or animal (EXPOSURE CALL) or a request for information (INFORMATION CALL) with no person or animal exposed to any foreign body, viral, bacterial, venomous, or chemical agent or commercial product.

The NPDS Products Database

The NPDS products database contains over 390,000 products ranging from viral and bacterial agents to commercial chemical and drug products. The products 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 (formerly known as Thomson Reuters (Healthcare) Inc.). A robust generic coding system categorizes the products data into 985 generic codes. These generic codes collapse into Non-Pharmaceutical (551) and Pharmaceutical (434) groups. These two groups are divided into Major (67) and Minor (170) categories. The generic coding schema undergoes continuous improvement through the work of the AAPCC – Micromedex Joint Coding Group. The group consists of AAPCC members and editorial and lexicon staff to meet best terminology practices. The generic code system provides enhanced report granularity as reflected in . The following 19 generic codes were introduced in 2011:

Table: Generic Codes Added in 2011.

Because the new codes were added at different times during the year, the numbers in for these generic codes do not reflect the entire year. For completeness certain of these categories require customized data retrieval until these categories have been in place for a year or more.

Methods

Characterization of Participating Poison Centers and Population Served

Fifty-seven participating centers submitted data to AAPCC through 31 December 2011. Fifty-four centers (95%) were accredited by AAPCC as of 1 July 2011. The entire population of the 50 states, American Samoa, the District of Columbia, Federated States of Micronesia, Guam, Puerto Rico, and the US Virgin Islands was served by the US PC network in 2011.Citation2,Citation3

The average number of human exposure cases managed per day by all US PCs was 6,395. Similar to other years, higher volumes were observed in the warmer months, with a mean of 6,685 cases per day in June compared with 6,138 per day in January. On average, US PCs received a call about an actual human exposure every 13.5 seconds.

Call Management – Specialized Poison Exposure Emergency Providers

Most PC operations management, clinical education, and instruction are directed by Managing Directors (most are PharmDs and RNs with American Board of Applied Toxicology [ABAT] board certification). Medical direction is provided by Medical Directors who are board-certified physician medical toxicologists. At some PCs, the Managing and Medical Director positions are held by the same person.

Calls received at US PCs are managed by healthcare professionals who have received specialized training in toxicology and managing exposure emergencies. These providers include medical and clinical toxicologists, registered nurses, doctors of pharmacy, pharmacists, chemists, hazardous materials specialists, and epidemiologists. Specialists in Poison Information (SPIs) are primarily registered nurses, PharmDs, and pharmacists. They work under the supervision of a Certified Specialist in Poison Information (CSPI). SPIs must log a minimum of 2,000 calls over a 12 month period to become eligible to take the CSPI examination for certification in poison information. Poison Information Providers (PIPs) are allied healthcare professionals. They manage information-type and low acuity (non-hospital) calls and work under the supervision of a CSPI. Of note is the fact that no nursing or pharmacy school offers a toxicology curriculum designed for PC work and SPIs must be trained in programs offered by their respective PC. Centers undergo a rigorous accreditation process administered by the AAPCC and must be reaccredited every 5 years.

NPDS – Near Real-time Data Capture

Launched on 12 April 2006, NPDS is the data repository for all of the US regional PCs. In 2011, all 57 of the 57 US PCs uploaded case data automatically to NPDS. All centers submitted data in near real-time, making NPDS one of the few operational systems of its kind. PC staff record calls contemporaneously in 1 of 4 case data management systems. Each center uploads case data automatically. The time to upload data for all PCs is 21.1 [6.19, 13.5] (median [25%, 75%]) minutes creating a real-time national exposure database and surveillance system.

The web-based NPDS software facilitates detection, analysis, and reporting of NPDS surveillance anomalies. System software offers a myriad of surveillance uses allowing AAPCC, its member centers and public health agencies to utilize NPDS US exposure data. Users are able to access local and regional data for their own areas and view national aggregate data. The application allows for increased “drill-down” capability and mapping via a geographic information system (GIS). Custom surveillance definitions are available along with ad hoc reporting tools. Information in the NPDS database is dynamic. Each year the database is locked prior to extraction of annual report data to prevent inadvertent changes and ensure consistent, reproducible reports. The 2011 database was locked on 25 October 2012 at 15:14 EDT.

Annual Report Case Inclusion Criteria

The information in this report reflects only those cases that are not duplicates and classified by the regional PC as CLOSED. A case is closed when the PC has determined that no further follow-up/recommendations are required or no further information is available. Exposure cases are followed to obtain the most precise medical outcome possible. Depending on the case specifics, most calls are “closed” within a few hours of the initial call. Some calls regarding complex hospitalized patients or cases resulting in death may remain open for weeks or months while data continue to be collected. Follow-up calls provide a proven mechanism for monitoring the appropriateness of management recommendations, augmenting patient guidelines and providing poison prevention education, enabling continual updates of case information as well as obtaining final/known medical outcome status to make the data collected as accurate and complete as possible.

Statistical Methods

All tables except and were generated directly by the NPDS web-based application and can thus be reproduced by each center. The figures and statistics in and were created using SAS JMP version 9.0.0 (SAS Institute, Cary, NC) on summary counts generated by the NPDS web-based application.

NPDS Surveillance

As previously noted, all of the active US PCs upload case data automatically to NPDS. This unique near real-time upload is the foundation of the NPDS surveillance system. This makes possible both spatial and temporal case volume and case-based surveillance. NPDS software allows creation of volume and case-based definitions. Definitions can be applied to national, regional, state, or ZIP code coverage areas. Geocentric definitions can also be created. This functionality is available not only to the AAPCC surveillance team, but to every regional PC. PCs also have the ability to share NPDS real-time surveillance technology with external organizations such as their state and local health departments or other regulatory agencies. Another NPDS feature is the ability to generate system alerts on adverse drug events and other drug or commercial products of public health interest like contaminated food or product recalls. Thus NPDS can provide real-time adverse event monitoring and surveillance for resilience response and situational awareness.

Surveillance definitions can be created to monitor a variety of volume parameters or case based definitions 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 390,000 entries. Surveillance definitions may be constructed using volume or case-based definitions with a variety of mathematical options and historical baseline periods from 1 to 11 years. NPDS surveillance tools include:

  • Volume Alert Surveillance Definitions

  • Total Call Volume

  • Human Exposure Call Volume

  • Animal Exposure Call Volume

  • Information Call Volume

  • Clinical Effects Volume (signs and symptoms, or laboratory abnormalities)

  • Case-Based Surveillance Definitions utilizing various NPDS data fields linked in Boolean expressions

○ Substance

○ Clinical Effects

○ Species

○ Medical Outcome and others

Incoming data is monitored continuously and anomalous signals generate an automated email alert to the AAPCC's surveillance team or designated regional PC or public health agency staff. These anomaly alerts are reviewed daily by the AAPCC surveillance team, the regional PC, or the public health agency that created the surveillance definition. When reports of potential public health significance are detected, additional information is obtained via the NPDS surveillance correspondence system or phone as appropriate from reporting PCs. The regional PC then alerts their respective state or local health departments. Public health issues are brought to the attention of the Health Studies Branch, Division of Environmental Hazards and Health Effects, National Center for Environmental Health, Centers for Disease Control and Prevention (CDC). This unique near real-time tracking ability is a unique feature offered by NPDS and the regional PCs.

AAPCC Surveillance Team clinical and medical toxicologists review surveillance definitions on a regular basis to fine-tune the queries. CDC, as well as State and local health departments with NPDS access as granted by their respective regional PCs, also have the ability to create surveillance definitions for routine surveillance tasks or to respond to emerging public health events.

Fatality Case Review and Abstract Selection

NPDS fatality cases can be recorded as DEATH or DEATH (INDIRECT REPORT). Medical outcome of death is by direct report. Death (indirect reports) reports are deaths that the PC acquired from medical examiners or media, but did not manage or answer any questions related specifically to that death.

Although PCs may report death as an outcome, the death may not be the direct result of the exposure. We define exposure-related fatality as a death judged by the AAPCC Fatality Review Team to be at least contributory to the exposure. The definitions used for the Relative Contribution to Fatality (RCF) classification are defined in Appendix B and the methods to select abstracts for publications is described in Appendix C. For details of the AAPCC fatality review process, see the 2008 annual report.Citation1

Pediatric Fatality Case Review

A focused Pediatric Fatality Review team, comprised 4 pediatric toxicologists, in this year evaluated cases in patients under 18 years of age. The panel reviewed the documentation of all such cases, with specific focus on the conditions behind the poisoning exposure and on finding commonality which might inform efforts at prevention. The 66 cases reviewed exhibited a bimodal age distribution. Exposures causing death in children ≤ 5 years of age were mostly coded as “Unintentional-General”, while those in ages over 12 years were mostly “Intentional”. Often the Reason Code did not capture the complexities of the case. For example, there were few mentions of details such as the involvement of law enforcement or child protective services. While there were some complete and informative reports, in many narratives the circumstances which preceded the exposure thought responsible for the death were unclear or absent. In response to these findings, the pediatric fatality review team developed and distributed Pediatric Narrative Guidelines for this year, with specific attention to the root cause of these cases. Poison centers are requested to heed these guidelines and the need for a more in-depth investigation of “causality.”

Results

Information Calls to Poison Centers

Data from 1,203,282 information calls to PCs in 2011 () was transmitted to NPDS, including calls in optional reporting categories such as prevention/safety/education (31,670), administrative (28,452) and caller referral (57,812).

shows that All Drug ID calls decreased dramatically in mid 2009, again in late 2010 and late 2011 (no regression was fit to these data). Law enforcement Drug ID Calls also showed a declining rate of increase. The most frequent information call was for Drug ID, comprising 715,544 calls to PCs during the year. Of these, 423,992 (59.3%) were identified as drugs with known abuse potential; however, these cases were categorized based on the drug's abuse potential without knowledge of whether abuse was actually intended.

While the number of Drug Information calls decreased 24.1% from 2010 (942,614 calls) to 2011 (715,544 calls), the distribution of these call types remained steady at 14.8% and 14.5%, respectively, of all information request calls. The most common drug information requests were in regard to therapeutic use and indications, followed by drug–drug interactions, questions about dosage and inquiries of adverse effects. Environmental inquiries comprised 1.9% of all information calls. Of these environmental inquiries, 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 5.6% of the requests with inquiries involving general toxicity the most common followed by questions involving food preparation practices, plant toxicity and safe use of household products.

Exposure Calls to Poison Centers

In 2011, the participating PCs logged 3,624,063 total encounters including 2,334,004 closed human exposure cases (), 80,266 animal exposures (), 1,203,282 information calls (), 6,243 human-confirmed non-exposures, and 268 animal-confirmed non-exposures. An additional 674 calls were still open at the time of database lock. The cumulative AAPCC database now contains almost 56 million human exposure case records (). A total of 14,560,932 information calls have been logged by NPDS since the year 2001.

Table 1A. AAPCC population: served and reported exposures (1983–2011).

Table 1B. Non-human exposures by animal type.

Table 1C. Distribution of information calls.

shows the human exposures, information calls and animal exposures by day since January 1, 2001. Second order (quadratic) least squares regression of these data shows a statistically significant departure from linearity (declining rate of calls since mid-2007) for Human Exposure Calls. Information Calls are declining more rapidly than the quadratic regression this year, and Animal Exposure Calls have likewise been declining since mid-2005.

Fig. 1. Human Exposure Calls, Information Calls and Animal Exposure Calls by Day since 1 January 2000. Black lines show least-squares second order regression–both linear and second order (quadratic) terms were statistically significant for each of the 3 regressions.

Fig. 1. Human Exposure Calls, Information Calls and Animal Exposure Calls by Day since 1 January 2000. Black lines show least-squares second order regression–both linear and second order (quadratic) terms were statistically significant for each of the 3 regressions.

Fig. 2. All Drug Identification and Law Enforcement Drug Identification Calls by Day since 1 January 2000. Black line shows least-squares second order regression–both linear and second order (quadratic) terms were statistically significant for the Law Enforcement Drug ID Calls.

Fig. 2. All Drug Identification and Law Enforcement Drug Identification Calls by Day since 1 January 2000. Black line shows least-squares second order regression–both linear and second order (quadratic) terms were statistically significant for the Law Enforcement Drug ID Calls.

A hallmark of PC case management is the use of follow-up calls to monitor case progress and medical outcome. US PCs made 2,785,633 follow-up calls in 2011. Follow-up calls were done in 46.8% of human exposure cases. One follow-up call was made in 23.0% of human exposure cases, and multiple follow-up calls (range 2–132) were placed in 23.8% of cases.

shows a graphic summary and analyses of Health Care Facility (HCF) Exposure and HCF Information calls. HCF Exposure Calls did not depart from linearity (continued to increase at a steady rate) while the rate of HCF Information Calls has been declining since early 2005. This linearly increasing use of the PCs for the more serious exposures (HCF calls) is important in the face of the declining growth of all exposure and information calls. The 2 May 2006 exposure data spike on the figure was the result of 602 children in a Midwest school reporting a noxious odor which caused anxiety, but resolved without sequelae.

Fig. 3. Health Care Facility (HCF) Exposure Calls and HCF Information Calls by Day since 1 January 2000. Black lines show least-squares first and second order regressions—linear regression for HCF Exposure Calls (second order term was not statistically significant) and second order regression for HCF Information Calls. All terms shown were statistically significant for each of the 2 regressions.

Fig. 3. Health Care Facility (HCF) Exposure Calls and HCF Information Calls by Day since 1 January 2000. Black lines show least-squares first and second order regressions—linear regression for HCF Exposure Calls (second order term was not statistically significant) and second order regression for HCF Information Calls. All terms shown were statistically significant for each of the 2 regressions.

(Nonpharmaceuticals) and (Pharmaceuticals) provide summary demographic data on patient age, reason for exposure, medical outcome, and use of a health care facility for all 2,334,004 human exposure cases, presented by substance categories.

Column 1: Name of the major, minor generic categories and their associated generic substance name.

Column 2: No. of Case Mentions (all exposures) in grey shading, displays the number of times the specific generic code was reported in all human exposure cases. If a human exposure case has multiple instances of a specific generic code it is only counted once.

Column 3: No. of Single 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 identified 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 outcome of Death or Death (indirect report). These death cases are not limited by the relative contribution to fatality.

and restrict the breakdown columns to single-substance cases. Prior to 2007, when multi-substance 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 single-substance exposures should increase precision and reduce misrepresentation of the results in this unique by-substance table. Single substance cases reflect the majority (90%) of all exposures. In contrast, only 42% of fatalities are single substance exposures ().

and tabulate 2,719,970 substance-exposures, of which 2,090,698 were single-substance exposures, including 1,071,939 (51.3%) nonpharmaceuticals and 1,018,759 (48.7%) pharmaceuticals. In 19.0% of single-substance exposures that involved pharmaceutical substances, the reason for exposure was intentional, compared to only 3.5% when the exposure involved a nonpharmaceutical substance. Correspondingly, treatment in a health care facility was provided in a higher percentage of exposures that involved pharmaceutical substances (28.8%) compared with nonpharmaceutical substances (15.1%). Exposures to pharmaceuticals also had more severe outcomes. Of single-substance exposure-related fatal cases, 521 (0.85%) were pharmaceuticals compared with 242 (0.02%) nonpharmaceuticals.

Age and Gender Distributions

The age and gender distribution of human exposures is outlined in and Children younger than 3 years of age were involved in 36.2% of exposures and children younger than 6 years accounted for approximately half of all human exposures (48.9%). A male predominance was found among cases involving children younger than 13 years, but this gender distribution was reversed in teenagers and adults, with females comprising the majority of reported exposures.

Caller Site and Exposure Site

As shown in , of the 2,334,004 human exposures reported, 73.2% of calls originated from a residence (own or other) but 93.6% actually occurred at a residence (own or other). Another 18.8% of calls were made from a health care facility. Beyond residences, exposures occurred in the workplace in 1.6% of cases, schools (1.2%), health care facilities (0.3%), and restaurants or food services (0.2%).

Table 2. Site of call and site of exposure, human exposure cases.

Table 3A. Age and gender distribution of human exposures.

Table 3B. Population-adjusted exposures by age group.

Table 4. Distribution of agea and gender for fatalities.b

Table 5. Number of substances involved in human exposure cases.

Exposures in Pregnancy

Exposure during pregnancy occurred in 7,834 women (0.34% of all human exposures). Of those with known pregnancy duration (n = 7,189), 29.9% occurred in the first trimester, 38.2% in the second trimester, and 31.9% in the third trimester. Most (72.7%) were unintentional exposures and 20.9% were intentional exposures. There was one death in a pregnant female in 2010.

Chronicity

Most human exposures, 2,069,586 (88.7%) were acute cases (single, repeated or continuous exposure occurring over 8 hours or less) compared to 1205 acute cases of 2765 fatalities (43.6%). Chronic exposures (continuous or repeated exposures occurring over > 8 hours) comprised 2% (48,753) of all human exposures. Acute-on-chronic exposures (single exposure that was preceded by a continuous, repeated, or intermittent exposure occurring over a period greater than eight hours) numbered 185,793 (8.0%).

Reason for Exposure

The reason category for most human exposures was unintentional (80.3%) with unintentional general (55.5%), therapeutic error (12.1%) and unintentional misuse (5.4%) of all exposures ().

Table 6A. Reason for human exposure cases.

Scenarios

Of the total 299,832 therapeutic errors, the most common scenarios for all ages included: inadvertent double-dosing (28.6%), wrong medication taken or given (15.3%), other incorrect dose (13.6%), doses given/taken too close together (9.6%), and inadvertent exposure to someone else's medication (8.5%). The types of therapeutic errors observed are different for each age group and are summarized in .

Table 6B. Scenarios for therapeutic errorsa by age.b

Reason by Age

Intentional exposures accounted for 15.8% of human exposures. Suicidal intent was suspected in 9.6% of cases, intentional misuse in 2.5% and intentional abuse in 2.7%. Unintentional exposures outnumbered intentional exposures in all age groups with the exception of ages 13–19 years (). Intentional exposures were more frequently reported than unintentional exposures in patients aged 13–19 years. In contrast, of the 1,158 reported fatalities with RCF 1–3, the majority reason reported for children ≤ 5 years was unintentional while most fatalities in adults (> 20 years) were intentional ().

Table 7. Distribution of reason for exposure by age.

Table 8. Distribution of reason for exposure and age for fatalities.a

Route of Exposure

Ingestion was the route of exposure in 83.2% of cases (), followed in frequency by dermal (7.0%), inhalation/nasal (6.1%), and ocular routes (4.3%). For the 1,158 exposure-related fatalities, ingestion (84.3%), inhalation/nasal (10.2%), and parenteral (4.6%) were the predominant exposure routes. Each exposure case may have more than one route.

Table 9. Route of exposure for human exposure cases.

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 defined as related, not related, or unknown if related. Clinical effects were coded in 852,963 (36.5%) cases. (17.9% had 1 effect, 9.5% had 2 effects, 5.1% had 3 effects, 2.1% had 4 effects, 0.9% had 5 effects, and 1.0% had > 5 effects coded). Of clinical effects coded, 79.1% were deemed related to the exposure, 9.4% were considered not related, and 11.5% were coded as unknown if related.

Case Management Site

The majority of cases reported to PCs were managed in a non–health care facility (69.9%), usually at the site of exposure, primarily the patient's own residence (). 1.7% of cases were referred to a health care facility but refused referral. Treatment in a health care facility was rendered in 26.4% of cases.

Table 10. Management site of human exposures.

Of the 615,869 cases managed in a health care facility, 295,110 (47.9%) were treated and released, 101,175 (16.4%) were admitted for critical care, and 65,845 (10.7%) were admitted to a noncritical unit.

The percentage of patients treated in a health care facility varied considerably with age. Only 11.3% of children ≤ 5 years or younger and only 13.3% of children between 6 and 12 years were managed in a health care facility compared to 50.1% of teenagers (13–19 years) and 41.1% of adults (age ≥ 20 years).

Medical Outcome

displays the medical outcome of human exposure cases distributed by age. Older age groups exhibit a greater number of severe medical outcomes. compares medical outcome and reason for exposure and shows a greater frequency of serious outcomes in intentional exposures.

Table 11. Medical outcome of human exposure cases by patient age.a

Table 12. Medical outcome by reason for exposure in human exposures.a

The duration of effect is required for all cases that report at least one clinical effect and have a medical outcome of minor, moderate or major effect (n = 523,353; 22.4% of exposures). demonstrates an increasing duration of the clinical effects observed with more severe outcomes.

Table 13. Duration of clinical effects by medical outcome.

Decontamination Procedures and Specific Antidotes

and outline the use of decontamination procedures, specific 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.

Table 14. Decontamination and therapeutic interventions.

Table 15. Therapy provided in human exposures by age.

Ipecac-induced emesis for poisoning continues to decline as shown in and . Ipecac was administered in only 98 (0.01%) pediatric exposures in 2011. The continued decrease in ipecac syrup use over the last 2 decades was likely a result of ipecac use guidelines issued in 1997 by the American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists and updated in 2004.Citation5,Citation6 In a separate report, the American Academy of Pediatrics concluded not only that ipecac should no longer be used routinely as a home treatment strategy, but also recommended disposal of home ipecac stocks.Citation7 A decline was also observed since the early 1990s for reported use of activated charcoal. While not as dramatic as the decline in use of ipecac, reported use of activated charcoal decreased from 3.7% of pediatric cases in 1993 to just 1.2% in 2011.

Table 16A. Decontamination trends (1985–2011).

Table 16B. Decontamination Trends: Total Human and Pediatric Exposures < = 5 Years (2011).a

Top Substances in Human Exposures

presents the most common 25 substance categories, listed by frequency of human exposure. This ranking provides an indication where prevention efforts might be focused, as well as the types of exposures PCs regularly manage. It is relevant to know whether exposures to these substances are increasing or decreasing.

Table 17A. Substance categories most frequently involved in human exposures (Top 25).

To better understand these relationships, we examined exposures per year over the last 11 years for the change over time for each of the 67 major generic categories via least squares linear regression. The exposure calls per year over this period were increasing for 40 and decreasing for 27 of the 67 categories. The change over time for the 11 yearly values was statistically significant (p < 0.05) for 51 of the 67 categories. shows the 25 categories which were increasing most rapidly. Statistical significance of the linear regressions can be verified by noting the 95% confidence interval on the rate of increase excludes zero for all 25 of these categories. shows the linear regressions for the top 4 increasing categories in .

Fig. 4. Change in Exposure Calls by Outcome from 2010 to 2011. The figure shows how the decrease of 94,530 in Human Exposure Calls divides among the 10 Medical Outcomes. The More Serious Exposures (Minor, Moderate, Major, and Death) all increased and their combined increase was 22,175 calls (23.5% of the 94,530 total decrease). The Less Serious Exposures (the other 6 outcome groups) decreased by 116,705 (− 123.5% of the 94,530 total decrease). *Excludes CONFIRMED NONEXPOSURES and INDIRECT DEATH.

Fig. 4. Change in Exposure Calls by Outcome from 2010 to 2011. The figure shows how the decrease of 94,530 in Human Exposure Calls divides among the 10 Medical Outcomes. The More Serious Exposures (Minor, Moderate, Major, and Death) all increased and their combined increase was 22,175 calls (23.5% of the 94,530 total decrease). The Less Serious Exposures (the other 6 outcome groups) decreased by 116,705 (− 123.5% of the 94,530 total decrease). *Excludes CONFIRMED NONEXPOSURES and INDIRECT DEATH.

Fig. 5. Human Exposure Call Increases by Year 2000–2011 – Top 4 Categories. Solid lines show least-squares linear regressions for the Human Exposure Calls per year for that category (□). Broken lines show 95% confidence interval on the regression.

Fig. 5. Human Exposure Call Increases by Year 2000–2011 – Top 4 Categories. Solid lines show least-squares linear regressions for the Human Exposure Calls per year for that category (□). Broken lines show 95% confidence interval on the regression.

Table 17B. Substance categories with the greatest rate of exposure increase (Top 25).

and present exposure results for children and adults, respectively, and show the differences between substance categories involved in pediatric and adult exposures.

Table 17C. Substance categories most frequently involved in pediatric (≤ 5 years) exposures (Top 25).a

Table 17D. Substance categories most frequently involved in adult (≥ 20 years) exposures (Top 25).a

reports the 25 categories of substances most frequently involved in pediatric (≤ 5 years) fatalities in 2011.

Table 17E. Substance categories most frequently involved in pediatric (≤ 5 years) deaths.a

reports the 25 Drug ID categories most frequently queried in 2011. Unknown is the 4th and Miscellaneous the 15th most often identified drug category. These categories include medications which could not be identified, indicating 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 17F. Substance categories most frequently identified in drug identification calls (Top 25).

reports the 25 substance categories most frequently reported in exposures involving pregnant patients.

Table 17G. Substance categories most frequently involved in pregnant exposuresa (Top 25).

Table 18. Categories associated with largest number of fatalities (Top 25).a

Changes from Last Year

shows the year-to-year changes for 2011 compared to 2010 for all encounters (− 8.3%), exposure calls (− 2.2%) and for several other major categories.

The graphic and bottom data display break down the change in exposure calls by outcome category. Although overall exposure calls have decreased by 51,808 calls (− 2.2%), there is a consistent increase in the exposures with a more serious outcome (moderate, major or death) and as a group increased by 10,889 encounters (+ 6.8%). Less serious calls (including Minor Effect) decreased by 62,698 encounters (− 3.4%).

Thus we see a consistent increase in exposure calls from HCFs () and for the more severe exposures (), despite a decrease in calls involving less severe exposures.

Distribution of Suicides

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 percent of exposures determined to be suspected suicides ranged from 31.3% to 54.3% and the percent of pediatric cases ranged from 1.5% to 3.2%. The relatively large change seen for 2011 reflects the large increase in death, indirect reports this year. Analyses of suicides and pediatric deaths for Direct and Indirect reports are shown in .

Table 19A. Comparisons of death data (1985–2011).a

Table 19B. Comparisons of direct and indirect death data (2006–2011).a

Plant Exposures

provides the number of times the specific plant was reported to NPDS (N = 47,561). The 25 most commonly involved plant species and categories account for 37.5% of all plant exposures reported. The top 3 categories in the table are essentially synonymous for unknown plant and comprise 11.5% (5,458/47,561) of all plant exposures. For a variety of reasons it was not possible to make a precise identification in these 3 groups. The top most frequent plant exposures where a positive plant identification was made were (descending order): Spathiphyllum species (Botanic name), Phytolacca americana (L.) (Botanic name), Ilex species (Botanic name), Philodendron (Species unspecified) and Euphorbia pulcherrima (Willd.) (Botanic name).

Table 20. Frequency of plant exposures (Top 25).a

Deaths and Exposure-related Fatalities

A listing of cases () and summary of cases (, , , , and ) are provided for fatal cases for which there exists reasonable confidence that the death was a result of that exposure (exposure-related fatalities). , , and and list all deaths, irrespective of the Relative Contribution to Fatality (RCF). Beginning in 2010, cases with outcome of Death, Indirect Report were not further reviewed by the AAPCC fatality review team and the RCF was determined by the individual poison center review team.

Table 21. Listing of fatal nonpharmaceutical and pharmaceutical exposures.

Table 22A. Demographic profile of SINGLE SUBSTANCE Nonpharmaceuticals exposure cases by generic category.

Table 22B. Demographic profile of SINGLE SUBSTANCE Pharmaceuticals exposure cases by generic category.

There were 1,262 death, indirect and 1,503 deaths. Of these 2,765 cases, 1,995 were judged exposure-related fatalities (RCF = 1-Undoubtedly responsible, 2-Probably responsible, or 3-Contributory). The remaining 770 cases were judged as follows: 95 as RCF = 4-Probably not responsible, 37 as 5-Clearly not responsible, and 638 as 6-Unknown.

Deaths are sorted in according to the category, then substance deemed most likely responsible for the death (Cause Rank), and then by patient age. The Cause Rank permits the regional PC to judge 2 or more substances as indistinguishable in terms of cause, e.g., 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 , a single substance was implicated in 90.0% of reported human exposures, and 10.0% of patients were exposed to 2 or more drugs or products. The exposure-related fatalities involved a single substance in 489 cases (42.2%), 2 substances in 260 cases (22.5%), 3 in 168 cases (14.5%), and 4 or more in the balance of the cases.

In , 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 = Death, Indirect report (occurred in 837, 42.0% of cases), p = prehospital cardiac and/or respiratory arrest (occurred in 576 of 1,995, 28.9% of cases), h = hospital records reviewed (occurred in 459, 24.8% of cases), a = autopsy report reviewed (occurred in 1,190, 59.6% of cases). The distribution of NPDS RCF was: 1 = Undoubtedly responsible in 677 cases (33.9%), 2 = Probably responsible in 1,088 cases (54.5%), 3 = Contributory in 2,330 cases (11.5%). The denominator for these percentages is 1,995.

All fatalities – all ages

presents the age and gender distribution for these 1,158 exposure-related fatalities (excluding death, indirect). The age distribution of reported fatalities is similar to that in past years with 70 (6.0%) of the fatalities in children (< 20 years old), 1,085 of 1,158 (93.7%) of fatal cases occurring in adults (age ≥ 20 years) and 3 (0.3%) of fatalities occurring in Unknown Age patients. Although children ≤ 5 years old were involved in the majority of exposures, the 20 fatalities comprised just 1.7% of the exposure-related fatalities. Most (72.3%) of the fatalities occurred in 20-to 59-year-old individuals.

lists each of the 1,995 human fatalities (including death, indirect report) along with all of the substances involved. Please note: the substance listed in column 3 of (alternate name) was chosen to be the most specific generic name based upon the Micromedex Poisindex product name and generic code selected for that substance. Alternate names are maintained in the NPDS for each substance involved in a fatality. The cross-references at the end of each major category section in 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 ).

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 acetaminophen combination products, lead this list followed by miscellaneous antidepressants, miscellaneous alcohols, acetaminophen alone, miscellaneous anticonvulsants, and miscellaneous stimulants and street drugs. Note that 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.

The first ranked substance () was a pharmaceutical in 1,689 (84.7%) of the 1,995 fatalities. These 1,689 first ranked pharmaceuticals included:

850 analgesics (134 methadone, 122 acetaminophen/hydrocodone, 120 oxycodone, 117 acetaminophen, 97 morphine, 61 fentanyl, 39 salicylate, 24 tramadol, 21 acetaminophen/hydrocodone, 16 acetaminophen/oxycodone)

148 antidepressants (45 amitriptyline, 17 bupropion, 16 bupropion (extended release), 15 (citalopram, 9 doxepin, 8 trazodone, 8 venlafaxine, 6 tricyclic antidepressant)

128 cardiovascular drugs (32 verapamil, 26 amlodipine, 16 cardiac glycoside, 12 diltiazem (extended release), 11 metoprolol, 9 atenolol, 8 diltiazem, 7 propanolol)

111 sedative/hypnotic/antipsychotics (38 alprazolam, 15 quetiapine, 8 clonazepam, 7 zolpidem, 5 clonazepam)

246 stimulants/street drugs (88 methamphetamine, 59 cocaine, 44 heroin, 24 amphetamines (bath salts), 7 10 methylenedioxymethamphetamine (MDMA), 4 phencyclidine, 3 THC homolog)

The exposure was acute in 778 (39.0%), A/C = acute on chronic in 270 (13.5%), C = chronic exposure in 93 (4.6%) and U = unknown in 854 (42.8%).

A total of 2,964 tissue concentrations for 1 or more related analytes were reported in 1,376 cases. Most of these (2,748) are listed in , while all tissue concentrations are available to the member centers through the NPDS Enterprise Reports. These 137 analytes included: 359 ethanol, 229 acetaminophen, 167 oxycodone, 158 alprazolam, 152 hydrocodone, 115 methadone, 111 morphine (free), 91 methamphetamine, 79 fentanyl, 70 salicylate, 58 benzoylecognine, 46 tramadol, 46 oxymorphone, and 44 cocaine.

Route of exposure was: Ingestion only in 1,338 cases (67.1%), inhalation/nasal only in 118 cases (5.9%), parenteral in 45 cases (2.3%). Most other routes were combination routes or unknown.

The Intentional exposure reason was: Suspected suicide in 737 cases (36.8%), Abuse in 774 cases (38.8%), and Misuse in 51 cases (2.6%). Unintentional exposure reason was: Environmental in 50 cases (2.5%), Therapeutic error in 28 cases (1.4%), and Misuse in 12 cases 0.6%), and Occupational in 11 (0.6%). Adverse drug reaction was the reason in 39 (2.0%).

Pediatric fatalities – age ≤ 5 years

Although children younger than 6 years were involved in the majority of exposures, they comprised 42 of 2,765 (1.5%) of fatalities. These numbers are similar to those reported since 1985 (, all RCFs and includes indirect deaths). (RCF 1,2,3, excludes indirect deaths) shows the percentage fatalities in children ≤ 5 years related to total pediatric exposures was 20/1,144,729 = 0.00367%. By comparison, 1,073/766,914 = 0.14% of all adult, exposures involved a fatality. Of these 20 pediatric fatalities, 17 (85.0%) were reported as unintentional and 1 (5.0%) were coded as resulting from malicious intent ().

The 25 fatalities in children ≤ 5 years old in (includes death, indirect reports and RCF 1–3) included 12 pharmaceuticals and 13 nonpharmaceuticals. The first ranked substances associated with these fatalities included: methamphetamine and methadone in 3 cases, hydrofluoric acid, lamp oil, smoke, in 2 cases each, and 13 other substances (1 each).

Pediatric fatalities – ages 6–12 years

In the age range 6–12 years, there were 6 reported fatalities, 1 of which was unintentional general, 2 where unintentional environmental, 1 was unintentional therapeutic error,1 was intentional abuse, and 1 unintentional misuse (). The 8 fatalities listed in (includes death, indirect reports and RCF 1–3) included: 3 smoke, 1 activated charcoal, 1 freon, 1 paint (aerosol), 1 methadone, and 1 sodium bicarbonate.

Adolescent fatalities – ages 13–19 years

In the age range 13–19 years, there were 44 reported fatalities including 40 intentional and 1 unintentional (). The 67 fatalities listed in (includes death, indirect reports and RCF 1–3) included 57 pharmaceuticals and 10 nonpharmaceuticals. The first ranked pharmaceuticals associated with these fatalities included: methadone (9 cases), heroin (5 cases), oxymorphone (4 cases each), acetaminophen/hydrocodone, alprazolam, methamphetamine, oxycodone (3 cases each), colchicine, methylenedioxymethamphetamine (MDMA), THC homolog, tramadol (2 cases each), and the balance 1 substance each. The first ranked nonpharmaceuticals associated with these fatalities included: freon in 4 cases, ethanol and smoke (2 cases each); and the balance 1 substance each.

Pregnancy and Fatalities

A total of 26 deaths of pregnant women have been reported from the years 2000 through 2011. The majority (22 of 26) were intentional exposures (misuse, abuse or suspected suicide). There was 1 death in a pregnant women reported to NPDS in 2011. A 19 year-old female, 20 weeks gestation, ingested an unknown amount of methamphetamine while fleeing police. She was agitated and combative in the ED, BP 170/80, HR 170, T 41.7°C. She suffered a cardiac arrest in the ED. She was intubated, resuscitated, lavaged, given activated charcoal, cooling measures, benzodiazepines for sedation, and admitted to the ICU. She regained no neurologic function, delivered a stillborn infant, and died on hospital day 3. The fatality was judged undoubtedly responsible to the methamphetamine.

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 definitions, 37 regional PCs utilize NPDS as part of their surveillance programs. Three state health departments plus CDC run surveillance definitions in NPDS. Since Surveillance Anomaly 1, generated at 2:00 pm EDT on 17 September 2006, over 191,000 anomalies have been detected. More than 1000 were confirmed as being of public health significance with regional PCs working collaboratively with their local and state health departments and in some instances CDC on the public health issues identified.

At the time of this report, 380 surveillance definitions run continuously, monitoring case and clinical effects volume and a variety of case-based definitions from food poisoning to nerve agents. These definitions represent the surveillance work by many regional 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.Citation8 Less controversial is the benefit to situational awareness that NPDS can provide.Citation9 Typical NPDS surveillance data detects a response to an event rather than event prediction. This aids in situational awareness and resilience during and after a public health event.

Discussion

The exposure cases and information requests reported by PCs in 2011 do not reflect 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 covers only those exposures which are reported to PCs.

NPDS 2000–2011 call volume data clearly demonstrate a continuing decrease in exposure calls. This decline has been apparent and increasing since mid-2007 and reflects 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 health care facility calls have continued a consistent increase. Possible contributors to the declining PC access include: declining US birth (especially since exposure rates are much higher in children ≤ 5 years of age), increasing use of text over voice communication, and increased use of and reliance on internet search engines and web resources. To meet our public health goals, poison centers 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 poison center. Likewise minor exposures may progress to more severe morbidity and mortality because of incorrect internet information or no telephone management. The net effect could be more severe poisoning outcomes because fewer people took advantage of poison center services, with a resultant increased burden on the national healthcare infrastructure.

NPDS regression analyses indicate that all analgesic exposures including opioids and sedatives are increasing year after year. This trend is shown in and . NPDS data mirror CDC data that demonstrate similar findings.Citation9 Thus NPDS provides a real-time view of these public health issues without the need for data source extrapolations.

One of the limitations of NPDS data has been the perceived lack of fatality case volume compared to other reporting sources. However, when change over time is studied, NPDS is clearly consistent with other public health fatality analyses. One of the issues leading to this concern is the fact that medical record systems seldom have common output streams. This is particularly apparent with the various electronic medical record systems available. It is important to build a federated approach similar to the one modeled by NPDS to allow data sharing, for example, between hospital emergency departments and other medical record systems including medical examiner offices nationwide. Enhancements to NPDS can promote interoperability between NPDS and electronic medical records systems to better trend poison-related morbidity and mortality in the US and internationally.

Summary

Unintentional and intentional exposures continue to be a significant cause of morbidity and mortality in the US. 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.

Changes in encounters in 2011 compared to 2010 shown in include:

  • Total encounters (all exposure and information calls) decreased by 8.3%;

  • All information calls decreased 17.9%, Drug ID calls decreased 24.1%, and human exposures decreased 2.2%;

  • Health care facility (HCF) information calls decreased 2.9% while HCF exposures increased 4.8%;

  • Human exposures with less serious outcomes decreased 3.4% while those with more serious outcomes (minor, moderate, major or death) increased 6.8%;

  • The categories of substance exposures increasing most rapidly are: analgesics, followed by sedative/hypnotics/antipsychotics, cardiovascular drugs, antihistamines.

These data support the continued value of poison center expertise and need for specialized medical toxicology information to manage the more severe exposures, despite a decrease in calls involving less severe exposures. Poison centers must consider newer communication approaches that match current public communication patterns in addition to the traditional telephone call.

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.

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 reflect only information provided when the public or healthcare professionals report an actual or potential exposure to a substance (e.g., an ingestion, inhalation, or topical exposure, etc.), 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).

Appendix A – Acknowledgments

The compilation of the data presented in this report was supported in part through the US Centers for Disease Control AAPCC Contract 200-2011-41767.

The authors wish to express their appreciation to the following individuals who assisted in the preparation of the manuscript: Katherine W. Worthen, Laura J. Rivers, and Regina R. Padilla.

The authors express their sincere gratitude to the staff at the AAPCC Central Office for their support during the preparation of the manuscript: Deborah A Carr, Med, Executive Director, Julie Tufts and the entire staff.

Poison Centers (PCs)

We gratefully acknowledge the extensive contributions of each participating PC and the assistance of the many health care providers who provided comprehensive data to the PCs for inclusion in this database. We especially acknowledge the dedicated efforts of the Specialists in Poison Information (SPIs) who meticulously coded 3,624,063 calls made to US PCs in 2011.

As in previous years, the initial review of reported fatalities and development of the abstracts and case data for NPDS was the responsibility of the staff at the 60 participating PCs. Many individuals at each center participated in the fatality case preparation. These toxicology professionals and their centers are:

Alabama Poison Center

Perry Lovely, MD, ACMT

John Fisher, PharmD, DABAT, FAACT

Lois Dorough, BSN, RN, CSPI

Arizona Poison and Drug Information Center

Keith Boesen, PharmD, CSPI

F. Mazda Shirazi, MS, MD, PhD, FACEP

Arkansas Poison & Drug Information Center

Henry F. Simmons, Jr., MD

Pamala R. Rossi, PharmD

Howell Foster, PharmD

Banner Good Samaritan Poison and Drug Information Center

Daniel Brooks, MD

Belinda Sawyers, RN, CSPI

Jane Klemens, RN, CSPI

Sharyn Welch, RN

Blue Ridge Poison Center

Christopher P. Holstege, MD

Nathan P. Charlton, MD

Heather A. Borek, MD

California Poison Control System – Fresno/Madera Division

Richard J. Geller, MD, MPH

California Poison Control System – Sacramento Division

Timothy Albertson, MD, PhD

Judith Alsop, PharmD

California Poison Control System – San Diego Division

Richard F. Clark, MD

Lee Cantrell, PharmD

Jean Lo, MD

Stephen Thornton, MD

Michael Durracq, MD

California Poison Control System – San Francisco

Kent R. Olson, MD

Susan Kim-Katz, PharmD

Raymond Ho, PharmD

Kathryn Meier, PharmD

Sandra Hayashi, PharmD

Derrick Lung, MD

Patil Armenian, MD

Freda Rowley, PharmD

Ilene Anderson, PharmD

Jo Ellen Dyer, PharmD

Elizabeth Birdsall, PharmD

Beth Manning, PharmD

Ben Tsutaoka, PharmD

Michelle Fleurat, MD

Timur Durrani, MD, MPH

Carolinas Poison Center

Michael C. Beuhler, MD

Marsha Ford, MD

Anna Rouse Dulaney, PharmD

William Kerns II, MD

Christine M. Murphy, MD

Steven J Walsh, MD

Central Ohio Poison Center

Hannah Hays, MD

Marcel J. Casavant, MD, FACEP, FACMT

Heath Jolliff, DO, FACEP, FACMT, FAAEM

Julie Lecky, BA

Henry Spiller, DABAT, FAACT

Julie Lecky, BA

Julee Fuller-Pyle

Central Texas Poison Center

Ryan Morrissey, MD

Vikhyat Bebarta, MD

Douglas J. Borys, PharmD, DABAT

Children's Hospital of MI Regional Poison Center

Cynthia Aaron, MD

Lydia Baltarowich, MD

Jeffrey Bargeon, MD

Bram Dolcourt, MD

Susan C. Smolinske, PharmD

Brandon Warrick, MD

Cincinnati Drug and Poison Information Center

Shan Yin, MD, MPH

Sara Brown, RN

Connecticut Poison Center

Charles McKay, MD

Kathy Hart, MD

Bernard C. Sangalli, MS

Florida/USVI Poison Information Center – Jacksonville

Thomas Kunisaki, MD, FACEP, ACMT

Florida Poison Information Center – Miami

Jeffrey N. Bernstein, MD

Richard S. Weisman, PharmD

Florida Poison Information Center – Tampa

Cynthia R. Lewis-Younger, MD, MPH

Pam Eubank, RN, CSPI

Shirley Rendon, MD, CSPI

Judy Turner, RN, CSPI

Georgia Poison Center

Robert Geller, MD

Brent W. Morgan, MD

Ziad Kazzi, MD

Stella Wong, DO

Gaylord P. Lopez, PharmD

Stephanie Hon, PharmD

John Devlin, MD

Soumya Pandalai, MD

Adam Pomerleau, MD

Mohan Punja, MD

Sarah Jane Reedy, MD

Rizwan Riyaz, MD

Sophia Sheikh, MD

Rachel Gorodetsky, PharmD

Sara Miller, PharmD

Hennepin Regional Poison Center

David J. Roberts, MD

Elisabeth F. Bilden, MD

Deborah L. Anderson, PharmD

Jon B. Cole, MD

Heather Ellsworth, MD

Laurie Willhite, PharmD, CSPI

Illinois Poison Center

Michael Wahl, MD

Sean Bryant, MD

Indiana Poison Center

James B. Mowry, PharmD

Gwenn Christianson, MSN, CSPI

R. Brent Furbee, MD

Iowa Statewide Poison Control Center

Sue Ringling, RN

Edward Bottei, MD

Kentucky Regional Poison Center

George M. Bosse, MD

Henry A. Spiller, MS, RN, DABAT, FAACT

Louisiana Poison Center

Mark Ryan, PharmD

Thomas Arnold, MD

Maryland Poison Center

Suzanne Doyon, MD, FACMT

Samantha Lee, PharmD

Mississippi Poison Control Center

Robert Cox, MD, PhD, DABT, FACMT

Christina Parker, RN, CSPI

Missouri Poison Center at SSM Cardinal Glennon

Children's Medical Center

Anthony Scalzo, MD

Shelly Enders, PharmD, CSPI

National Capital Poison Center

Cathleen Clancy, MD, FACMT

Nicole Reid, RN, BA, BSN, MEd, CSPI

Nebraska Regional Poison Center

Claudia Barthold, MD

Ronald I. Kirschner, MD

New Jersey Poison Information and Education

System

Steven M. Marcus, MD

Bruce Ruck, PharmD

New Mexico Poison and Drug Information Center

Steven A. Seifert, MD, FAACT, FACMT

Blaine E. (Jess) Benson, PharmD, DABAT

New York City Poison Control Center

Maria Mercurio-Zappala, MS, RPh

Robert S. Hoffman, MD

Lewis Nelson, MD

Fiona Garlich, MD

Jeff Lapoint, DO

Colleen Rivers, MD

Betty Chen, MD

Lauren Shawn, MD

Hong Kim, MD

North Texas Poison Center

Brett Roth, MD, ACMT, FACMT

Melody Gardner, RN, MSN, CCRN

Northern Ohio Poison Center

Alfred Aleguas, BS Pharm, PharmD

Adrianne Grendzynski, RN, BSN, CSPI

Danielle Richardson, RN, BSN, CSPI

Susan Scruton, RN, BSN, CSPI

Northern New England Poison Center

Jane Clark

Tamas Peredy, MD

Oklahoma Poison Control Center

William Banner, Jr., MD, PhD, ABMT

Scott Schaeffer, RPh, DABAT

Oregon Poison Center

Zane Horowitz, MD

Sandra L. Giffin, RN, MS

Palmetto Poison Center

William H. Richardson, MD

Jill E. Michels, PharmD

Pittsburgh Poison Center

Kenneth D. Katz, MD

Rita Mrvos, BSN

Edward P. Krenzelok, PharmD

Puerto Rico Poison Center

José Eric Dîaz-Alcalá, MD

Andrés Britt, MD

Jamie L Nelsen, PharmD, DABAT

Elba Hernández, RN

Regional Center for Poison Control and Prevention Serving Massachusetts and Rhode Island

Michele Burns Ewald, MD

Dennis Wigandt, Pharm D

Russ Berger, MD

May Yen, MD

Regional Poison Control Center – Children's Hospital of Alabama

Erica Liebelt, MD, FACMT

Michele Nichols, MD

Sherrel Brooks, RN, CSPI

Ann Slattery, DrPH, DABAT

Diane Smith, RN, CSPI

Rocky Mountain Poison & Drug Center

Alvin C. Bronstein, MD, FACEP, FACMT

Christopher Hoyte, MD

Jeena Jacob, MD

Joseph Maddry, MD

Daniel Sessions, MD

Sam Wang, MD

Shireen Banerji, PharmD, DABAT

Carol Hesse, RN, CSPI

Regina R. Padilla

South Texas Poison Center

Cynthia Abbott-Teter, PharmD

Douglas Cobb, RPh

Heather N. Dellerman, MPH

Miguel C. Fernandez, MD

George Layton, MD

C. Lizette Villarreal, MA

Southeast Texas Poison Center

Wayne R. Snodgrass, MD, PhD, FACMT

Jon D. Thompson, MS, DABAT

Jean L. Cleary, PharmD, CSPI

Tennessee Poison Center

John G. Benitez, MD, MPH

Saralyn Williams, MD

Donna Seger, MD

Texas Panhandle Poison Center

Shu Shum, MD

Jeanie E. Jaramillo, PharmD

Cristie Johnston, RN, CSPI

The Poison Control Center at the Children's Hospital of Philadelphia

Allison A. Muller, PharmD

Kevin Osterhoudt, MD

University of Kansas Hospital Poison Control

Center

Tama Sawyer, PharmD, DABAT

Stephen Thornton, MD

Upstate NY Poison Center

Prashant Joshi, MD

Jeanna M. Marraffa, PharmD

Alexander Garrard, PharmD

Christine M. Stork, PharmD

Ross Sullivan, MD

Timothy Wiegand, MD

Ashley Webb, PharmD

Utah Poison Control Center

Martin Caravati, MD, MPH

Virginia Poison Center

Rutherfoord Rose, PharmD

Kirk Cumpston, DO

Brandon Wills, DO

Paul Stromberg, MD

Washington Poison Center

William T. Hurley, MD, FACEP

David Serafin, CPIP

West Texas Regional Poison Center

John F. Haynes, Jr., MD, ABEM, ABMT

Stephen W. Borron, MD, MS, FACEP, FACMT

Leo Artalejo III, PharmD

Hector L. Rivera, RPh

West Virginia Poison Center

Elizabeth J. Scharman, PharmD, DABAT, BCPS, FAACT

Anthony F. Pizon, MD, ABMT

Wisconsin Poison Center

David D. Gummin, MD

Lori Rohde, RN, CSPI

AAPCC Fatality Review Team

The Lead and Peer review of the 2011 fatalities was carried out by the 38 individuals listed here. The authors and the AAPCC wish to express our appreciation for their volunteerism, dedication, hard work and good will in completing this task in a limited time.

Alfred Aleguas Jr, PharmD, DABAT, Northern Ohio Poison Center

Anna Rouse Dulaney*, PharmD, DABAT, Carolinas Poison Center

Ann-Jeannette Geib*, MD, FACEP, Assistant Professor of Emergency Medicine UMDNJ-Robert Wood Johnson Medical School New Brunswick, NJ

Bernard C Sangalli*, MS, DABAT, Connecticut Poison Center

Charles McKay, MD, Associate Medical Director, Connecticut Poison Control Center, University of Connecticut School of Medicine

Christine Murphy, MD, Carolinas Poison Center

Curtis Elko, CSOI, Washington Poison Center, Seattle

Cynthia Lewis-Younger, MD, MPH, Florida Poison Information Center - Tampa

Daniel Brooks, MD, Banner Good Samaritan Medical Center, Phoenix

David D Gummin, MD, Wisconsin Poison Center

Diane Calello, MD, New Jersey Poison Information and Education System

Elizabeth J Scharman, PharmD, DABAT, BCPS, FAACT, West Virginia Poison Center

Hannah Hays, MD, Central Ohio Poison Center, Columbus

Henry Spiller, MS, DABAT, FAACT, Kentucky Regional Poison Center, Louisville

Howell Foster, PharmD, ABAT, Arkansas P&DIC

Jan Scaglione, PharmD, DBAT, Cincinnati Drug and Poison Information Center

Jeffrey S Fine, MD, NYU School of Medicine/Bellevue Hospital

Jennifer Lowry, MD, Division of Clinical Pharmacology and Medical Toxicology, Children’s Mercy Hospital, Kansas City, MO

Jill E. Michels, PharmD, DABAT, Managing Director, Palmetto Poison Center, SC

Judith A Alsop, PharmD, DABAT, California Poison Control System - Sacramento Division

Karen E Simone, PharmD, DABAT, Director, Northern New England Poison Center, Maine Medical Center

Kathryn Meier, PharmD, DABAT, Senior Toxicology Management Specialist, California Poison Control System, San Francisco Division

Kathy Hart, MD, Connecticut Poison Control Center

L Keith French, MD, Oregon Poison Center

Maria Mercurio-Zappala, RPh, MS, DABAT, FAACT, NYC PCC,

Mark Su, MD, FACEP, FACMT, North Shore University Hospital, NY

Michael Beuhler, MD, Medical Director, Carolinas Poison Center

Mike Levine*, MD, Banner Good Samaritan Medical Center, Phoenix

Nathanael McKeown*, DO, Oregon Poison Center

Rachel Gorodetsky, PharmD, D’Youville College School of Pharmacy, University of Rochester Medical Center

Rais Vohra, MD, California Poison Control System, Fresno/Madera

Richard J. Geller, MD, MPH, Medical and Managing Director, California Poison Control System, Fresno/Madera

Robert B Palmer, PhD, DABAT, Toxicology Associates, Denver, CO; Rocky Mountain Poison and Drug Center, Denver, CO

Robert Goetz, PharmD, DBAT, Cincinnati Drug and Poison Information Center

Steven M. Marcus, MD, NJ Poison Information and Education System, Departments of Preventive Medicine and Community Health and Pediatrics, NJ Medical School, University of Medicine and Dentistry of NJ.

Susan Smolinske, PharmD, Children's Hospital of Michigan RPCC, Detroit

Timothy Wiegand*, MD, Director of Toxicology, University of Rochester, Medical Center and Strong Memorial Hospital; Consultant Toxicologist, SUNY Upstate Poison Center

William Hurley, MD, Washington Poison Center, Seattle

*These reviewers further volunteered to read the top ranked 200 abstracts and judged to publish or omit each.

AAPCC Micromedex Joint Coding Group

Chair: Elizabeth J. Scharman, PharmD, DABAT, BCPS, FAACT

Alvin C. Bronstein, MD, FACEP, FACMT

Christina Davis, PharmD

Sandy Giffin, RN, MS

Kendra Grande, RPh

Katherine M. Hurlbut, MD

Wendy Klein-Schwartz, PharmD, MPH

Fiona McNaughton

Susan C. Smolinske, PharmD

AAPCC Rapid Coding Team

Chair: Alvin C. Bronstein, MD, FACEP, FACMT

Elizabeth J. Scharman, PharmD, DABAT, BCPS, FAACT

Jay L. Schauben, PharmD, DABAT, FAACT

Susan C. Smolinske, PharmD

AAPCC Surveillance Team

NPDS surveillance anomalies are analyzed daily by a team of 10 medical and clinical toxicologists working across the country in a distributed system. These dedicated professionals interface with the Health Studies Branch, Division of Environmental Hazards and Health Effects, National Center for Environmental Health, Centers for Disease Control and Prevention (CDC) and the PCs on a regular basis to identify anomalies of public health significance and improve NPDS surveillance systems:

Alfred Aleguas, Pharm D, DABAT

S. David Baker, PharmD, DABAT

Director, Alvin C. Bronstein, MD, FACEP, FACMT

Blaine (Jess) Benson, PharmD, DABAT

Douglas J. Borys, PharmD, DABAT

John Fisher, PharmD, DABAT, FAACT

Jeanna M. Marraffa, PharmD, DABAT

Maria Mercurio-Zappala, RPH, MS, DABAT, FAACT

Henry A. Spiller, MS, DABAT, FAACT

Richard G. Thomas, Pharm D, DABAT

Regional Poison Center (PC) Fatality Awards

Each year the AAPCC and the Fatality Review team recognized several regional PCs for their extra effort in their preparation of fatality reports and prompt responses to reviewer queries during the review process. The awards were presented at the October 2012, North American Congress of Clinical Toxicology meeting in Las Vegas, NV.

First Center to Complete all Cases (28-Dec 2011, last of 16 cases), West Virginia Poison Center (Charleston)

Largest Number with Autopsy Reports (35 of 90 cases), Carolinas Poison Center (Charlotte)

Highest Percentage with Autopsy Reports (75% of 53 cases), Maryland Poison Center (Baltimore)

Largest Number of INDIRECT cases (771 of 1087 total cases reported for 2011), Oklahoma Poison Control Center (Oklahoma City)

Highest Overall Quality of Reports (9.93 of possible 13 for 24 cases), Central Ohio Poison Center (Columbus)

Greatest improvement in Overall Quality of Reports (5.16 increase from 4.78), Central Ohio Poison Center (Columbus)

Most Abstracts Published in last year's Annual report (11 of the 80 published narratives), Carolinas Poison Center (Charlotte)

Most Helpful Regional Poison Center Staff (based on survey of AAPCC review team), Marcel Casavant, Central Ohio Poison Center (Columbus)

honorable mention, Carol Hesse, Rocky Mountain Poison & Drug Center

Appendix B – Data Definitions

Reason for Exposure

NPDS classifies all calls as either EXPOSURE (concern about an exposure to a substance) or INFORMATION (no exposed human or animal). A call may provide information about one or more exposed person or animal (receptors).

Specialists in Poison Information (SPIs) coded the reasons for exposure reported by callers to PCs according to the following definitions:

Unintentional general: All unintentional exposures not otherwise defined below.

Environmental: Any passive, non-occupational exposure that results from contamination of air, water, or soil. Environmental exposures are usually caused by manmade contaminants.

Occupational: An exposure that occurs as a direct result of the person being on the job or in the workplace.

Therapeutic error: An unintentional deviation from a proper therapeutic regimen that results in the wrong dose, incorrect route of administration, administration to the wrong person, or administration of the wrong substance. Only exposures to medications or products used as medications are included. Drug interactions resulting from unintentional administration of drugs or foods which are known to interact are also included.

Unintentional misuse: Unintentional improper or incorrect use of a nonpharmaceutical substance. Unintentional misuse differs from intentional misuse in that the exposure was unplanned or not foreseen by the patient.

Bite/sting: All animal bites and stings, with or without envenomation, are included.

Food poisoning: Suspected or confirmed food poisoning; ingestion of food contaminated with microorganisms is included.

Unintentional unknown: An exposure determined to be unintentional, but the exact reason is unknown.

Suspected suicidal: An exposure resulting from the inappropriate use of a substance for reasons that are suspected to be self-destructive or manipulative.

Intentional misuse: An exposure resulting from the intentional improper or incorrect use.

Medical Outcome

No effect: The patient did not develop any signs or symptoms as a result of the exposure.

Minor effect: The patient developed some signs or symptoms as a result of the exposure, but they were minimally bothersome and generally resolved rapidly with no residual disability or disfigurement. A minor effect is often limited to the skin or mucus membranes (e.g., self-limited gastrointestinal symptoms, drowsiness, skin irritation, first-degree dermal burn, sinus tachycardia without hypotension, and transient cough).

Moderate effect: The patient exhibited signs or symptoms as a result of the exposure that were more pronounced, more prolonged, or more systemic in nature than minor symptoms. Usually, some form of treatment is indicated. Symptoms were not life-threatening, and the patient had no residual disability or disfigurement (e.g., corneal abrasion, acid-base disturbance, high fever, disorientation, hypotension that is rapidly responsive to treatment, and isolated brief seizures that respond readily to treatment).

Major effect: The patient exhibited signs or symptoms as a result of the exposure that were life-threatening or resulted in significant residual disability or disfigurement (e.g., repeated seizures or status epilepticus, respiratory compromise requiring intubation, ventricular tachycardia with hypotension, cardiac or respiratory arrest, esophageal stricture, and disseminated intravascular coagulation).

Death: The patient died as a result of the exposure or as a direct complication of the exposure.

Not followed, judged as nontoxic exposure: No follow-up calls were made to determine the outcome of the exposure because the substance implicated was nontoxic, the amount implicated was insignificant, or the route of exposure was unlikely to result in a clinical effect.

Not followed, minimal clinical effects possible: No follow-up calls were made to determine the patient's outcome because the exposure was likely to result in only minimal toxicity of a trivial nature. (The patient was expected to experience no more than a minor effect.).

Unable to follow, judged as a potentially toxic exposure: The patient was lost to follow-up, refused follow-up, or was not followed, but the exposure was significant and may have resulted in a moderate, major, or fatal outcome. Unrelated effect: The exposure was probably not responsible for the effect.

Confirmed nonexposure: This outcome option was coded to designate cases where there was reliable and objective evidence that an exposure initially believed to have occurred actually never occurred (e.g., all missing pills are later located). All cases coded as confirmed nonexposure are excluded from this report.

Death, indirect report: Death, indirect report are deaths that the poison center acquired from medical examiner or media, but did not manage nor answer any questions about the death.

Relative Contribution to Fatality (RCF)

The definitions used for the Relative Contribution to Fatality (RCF) classification were as follows:

Undoubtedly responsible - In the opinion of the CRT the Clinical Case Evidence establishes beyond a reasonable doubt that the SUBSTANCES actually caused the death.

Probably responsible - In the opinion of the CRT the Clinical Case Evidence suggests that the SUBSTANCES caused the death, but some reasonable doubt remained.

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 insufficient to impute or refute a causative relationship for the SUBSTANCES in this death.

Appendix C – Abstracts of Selected Cases

Selection of Abstracts for Publication

The abstracts included in Appendix C were selected for publication in a 3-stage process consisting of qualifying, ranking and reading. Qualifying was based on the RCF -- only RCF = 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 * 4.4 + Postmortem * 7.6 + Blood levels * 6.9 + Quality/Completeness * 6.4 + Novelty/Educational value * 6.0. Scores were normalized (z-score) within each reviewer before the final weighting: 33% for 1/N and 67% for weighted case scores.

The top ranked abstracts (200 + 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 5 or more of 8 publish votes were selected, further edited and cross-reviewed by the 2 managers.

Abstracts

Abstracts of the cases were selected (see Selection of Abstracts for Publication, above) from the human fatalities judged related to be an exposure as reported to US PCs in 2010. 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 1. Acute ethanol ingestion: undoubtedly responsible.

Scenario/Substances: A 4-y/o black female was found unresponsive in bed by her father around midnight, with a bottle of rum on the floor near her bed. The bottle was missing and suspected to have been ingested by the 4-y/o sometime that evening.

Past Medical History: No known past medical history, did not take any medications or herbal/dietary supplements.

Physical Exam: 4-y/o female arrived with asystole cardiac arrest. She was intubated and resuscitated but remained unresponsive, acidotic, tachycardic, and became hypotensive. Right pupil unreactive, left pupil sluggishly reactive.

Laboratory Data: ABG-pH 6.7/pCO2 45/pO2 94,

Alk phos 365, bilirubin 0.3, Ca 8.7, AST 591, ALT 1296, ethanol 272 mg/dL; salicylate and acetaminophen not detected. UDS negative.

Clinical Course: After resuscitation, the patient was transported to a tertiary care hospital via helicopter ˜4 hrs after being first found. Prior to transfer, the patient was given D5NS IV for volume replacement and management of hypoglycemia. Hemodialysis was also considered, but the patient was too hypotensive at the time. She was admitted to the PICU and given dopamine and sodium bicarbonate boluses. The child remained acidotic with pH < 6.9 and hypoglycemic with glu 45 despite IV dextrose. ˜7 hrs after being found, the patient had cardiac arrest from which she could not be resuscitated.

Autopsy Findings: The antemortem blood alcohol measured at the crime laboratory was 0.202 g/L and the AST to ALT ratio was > 2. Liver revealed diffuse hepatic microsteatosis; subdural/subarachnoid hemorrhage and cortical contusions of frontal lobes; subcutaneous hemorrhage in posterior neck and back. (injuries to head, neck, back not thought to be severe enough to have caused death); mildly elevated 17 hydroprogesterone (8 ng/ml); paratubal cysts.

Case 31. Acute methanol ingestion: undoubtedly responsible.

Scenario/Substances: A 41y/o male with a history of alcohol abuse had been drinking at home and his family left him in a state that they assumed was typical intoxication. When they returned several hours later he was unresponsive. The family called EMS, who found the patient to have agonal breathing, pupils small and fixed, T 32.8°C. He was transported to the ED.

Past Medical History: Alcohol abuse.

Physical Exam: He was unresponsive, with fixed, small pupils.

Laboratory Data: At the initial ED: K 6.0, HCO3 6.5, Cr 2.1, pH 6.6.

Clinical Course: At the initial ED, he had 1 generalized seizure and was hypotensive. He was intubated and placed upon on dopamine for hypotension. He was then transferred to a tertiary care hospital where he was found to be unresponsive, pupils 2 mm and unreactive bilaterally, HR 130–140, T 34.1°C. He was receiving dopamine, norepinephrine, and sodium bicarbonate for hypotension. His urine fluoresced under a black light indicating the presence of fluorescein and he was started on fomepizole at 15 mg/kg IV. He also received thiamine, pyridoxine, and folic acid. His laboratory results were:

Ca 7.6, lactate 10.5, PT 11.0, INR 1.0, ABG-pH 6.94/pCO2 52/pO2 428/HCO3 11/BE -21, O2 sat 100%. HR 133, BP 114/47, EKG QRS 100, QT/QTc 336/500. Repeat labs showed HCO3 14, anion gap 17; pH 7.15, BE -15. Methanol 620 mg/dL, ethylene glycol negative 2 hr later methanol 485 mg/dL. After 5 hr of dialysis, his methanol level was 72 mg/dL without clinical improvement, HR 106, BP 138/84, RR 10, O2 sat 95%. On Day 4 methanol was not detected, but, he remained unresponsive with fixed pupils and no corneal, cough, or gag reflexes. Head CT showed cerebral edema with evidence of transtentorial and impending cerebellar tonsillar herniation. An apnea test showed no signs of respiratory effort after 8 min. He was declared brain dead, comfort measures were instituted and he expired 25 min later.

Autopsy Findings: No autopsy was done.

Case 110. Acute methanol and organophosphate ingestion: undoubtedly responsible.

Scenario/Substances: A 55-y/o male was brought to the ED by police complaining of abdominal pain and diarrhea. The previous day, police had been chasing him on foot, and the patient hid in a wooded area prior to capture. While climbing over a fence he had sustained a neck laceration that was stapled in the ED. He had been observed carrying a container, but the container was not recovered. The next day he was brought back to the ED because of profuse diarrhea and abdominal pain. The patient denied ingestion. He had been in a police holding cell for about a day before the second ED visit.

Past Medical History: Hepatitis C, alcohol and methamphetamine abuse, but none for the last 6 months. No regular medications.

Physical Exam: BP 133/80, HR 104, RR 14. T 34.9°C (tympanically), O2 sat 97% on room air. Patient was noted to smell of paint thinner. Pupils miotic but reactive, Oral mucosa dry. Neck: Supple, 1 cm laceration stapled the previous day, heart and lungs unremarkable, abdomen soft with mild diffuse tenderness and no rebound, bowel sounds present, sleepy but oriented × 3.

Laboratory Data: WBC 20.6, Hgb 16.7, Hct 49.3, platelets 228, PTT 28, INR 1.1, ABG-pH 7.10/pCO2 18/pO2 121 on room air

Methanol 40 mg/dL ethylene glycol, isopropanol, acetone not detected.

Clinical Course: The patient received oral vancomycin and IV metronidazole for presumed C. difficile enterocolitis. He became progressively more obtunded and was intubated. A sodium bicarbonate infusion was begun for high anion gap academia. Methanol was detected and the patient received 6 hr of hemodialysis (no fomepizole was given). Repeat methanol was < 10 mg/dL. The patient remained minimally responsive despite correction of acidosis. A brain MRI was unremarkable. Based on the prognosis the family opted for institution of comfort measures and he expired on Day 8. Six weeks after the patient expired, police investigators located a 355 mL container about half full of gas line antifreeze (99% methanol). A second 355 mL container was about ¼ full of chlorpyrifos.

Autopsy Findings: Bilateral acute bronchopneumonia with hemorrhagic pulmonary edema, and multiple lung abscesses; acute cerebral edema and congestion. Methanol was not detected, and there was no testing for organophosphates or cholinesterase activity.

Case 112. Acute ethylene glycol ingestion: probably responsible.

Scenario/Substances: A 59-y/o male was seen in the urgent care center for dyspnea, given a bronchodilator, and sent to the ED when his dyspnea persisted. He had been drinking heavily the night before, but there was no history of other acute ingestion of medications or toxins.

Past Medical History: Hypertension, hyperlipidemia, obesity, depression, and previous suicide attempts × 2.

Physical Exam:. In the ED ee was alert and anxious; BP 215/114, HR 106, RR 32, T 37 C, O2 sat 96% on room air. His chest was clear. There were no focal neurological findings and no signs of leg or calf swelling.

Laboratory Data: ABG-pH 6.82/PCO2 44/PO2 132

Lactate > 30 mmol/L, CK 3000, serum ketones negative, serum acetaminophen and salicylate not detected. UDS negative, CxR perihilar infiltrates suggestive of failure vs. pneumonia. Urinalysis was positive for a small amount of blood on dipstick and the presence of calcium phosphate crystals on microscopic exam.

Clinical Course: In the ED he received lorazepam for anxiety, but then he showed decreased respiratory effort and became cyanotic so he was intubated and placed on a ventilator. IV fluids and sodium bicarbonate were given and he was admitted to the ICU. On Day 2 his readings were BUN 15, Cr 2.94. Ethylene glycol from admission came back 38 mg/dL and he was started on fomepizole and hemodialysis. He remained unconscious and head CT Day 3 showed loss of grey-white matter differentiation in the occipital lobe with low attenuation in central cranial structures. An MRI was consistent with global anoxic brain injury. He remained unresponsive over the next week, the family opted for institution of comfort measures and he expired.

Autopsy Findings: Kidney and liver showed geographic patterns of discoloration, which is suggestive of infarcts. The heart showed cardiomegaly, biventricular hypertrophy, severe atherosclerosis, and old infarct scars. There was severe bilateral pulmonary congestion and edema. There were multiple cerebrocortical infarcts. The coroner determined the cause of death to be acute ethylene glycol toxicity.

Case 115. Acute disc battery ingestion: undoubtedly responsible.

Scenario/Substances: A 4-y/o female was found unresponsive, pulseless, and apneic.

Past Medical History: Previously healthy.

Physical Exam: Comatose, with blood coming from mouth and nares.

Clinical Course: Child was brought to the ED as a suspected trauma. During resuscitation a chest radiograph was obtained to check positioning of the endotracheal tube and a button battery was noted in the esophagus. She received mechanical ventilation, IV fluids, epinephrine, blood transfusion, and was taken to operating room. An aorto-esophageal fistula was found, but the child could not be resuscitated.

Autopsy Findings: Esophagus to aorta fistula from erosion due to button battery.

Case 117. Acute crotalinae envenomation bite/sting: contributory.

Acute envenomation by Mojave rattlesnake (Crotalus scutulatus): contributory

Scenario/Substances: A physician reported a 54-y/o male reportedly bitten by a Mojave rattlesnake 2 days earlier. The patient had been working at railroad in a rural area late at night picking up trash when he was bitten. He developed symptoms consistent with an allergic reaction and was treated by EMS with diphenhydramine and epinephrine. His co-worker reported that he had altered mental status soon after the bite.

Past Medical History: Hypertension, diabetes, hyperlipidemia, previous traumatic brain injury, post-traumatic stress disorder.

Physical Exam: Bilateral puncture wounds to the hands with bilateral hand swelling.

Laboratory Data: BUN 59, Cr 3.6, INR “normal”; Day 2 post envenomation: Cr 6.7, phos 6.08, lactate 4.0, ionized Ca 3.3, PT 14.4, INR 1.49, Mg 1.7.

Clinical Course: The patient was treated with antivenin (Polyvalent Immune Fab –4 vials on Day 1 and 10 vials on Day 2). He had no further coagulation abnormalities or significant progression of swelling. When he arrived at the ED, he had a large upper GI bleed and developed multi-organ system failure including acute renal failure and hypoxia refractory to intubation and ventilation with 100% O2. A CT chest showed no pulmonary emboli. The patient expired of multi-organ system failure on Day 6.

Autopsy Findings: Not performed.

Case 120. Acute-on-chronic, epinephrine ingestion: probably responsible.

Scenario/Substances: This 28-y/o female used 30 doses of her epinephrine CFC inhaler, presumably to treat bronchospasm. She had a generalized seizure on that day and another on the following day. EMS was called to her home because of the recurrent convulsion, and they witnessed a generalized seizure and gave diazepam 5 mg IV.

Past Medical History: Bronchospasm, depression. No seizure history. Medications: paroxetine, epinephrine CFC inhaler.

Physical Exam: Nonverbal, but opened eyes after stimuli. Pupils 2 mm and sluggish, BP 111/82, HR 100–130 s; RR 26.

Laboratory Data: Metabolic panel was normal, except her K was 3.2. Salicylate 5.3 mg/dL, ethanol and acetaminophen were not detected. EKG showed sinus tachycardia with prolonged QTc 508.

Clinical Course: In the ED, her mental status worsened, becoming responsive only to painful stimuli. She had an additional seizure, and was given lorazepam 4 mg IV and loaded with 1 IV fosphenytoin. A CT and MRI of the brain showed basilar artery occlusion and had a large ischemic stroke. She was endotracheally intubated, and air-transport to a tertiary-care center where she underwent a successful cerebral angiogram and thrombectomy. On Day 2, she developed cerebral edema with herniation, brain death was declared, comfort measures were instituted, she expired, and organs were harvested.

Autopsy Findings: No autopsy was performed.

Case 124. Acute cyanide injection: undoubtedly responsible.

Scenario/Substances: A 33-y/o healthy female went to her boyfriend's house to collect her things, while her brother waited outside. The boyfriend, a jeweler, stabbed the patient in the buttock with a syringe containing clear liquid and then drank from a cup containing clear liquid. The patient cried out for her brother, who ran upstairs and called EMS, who found the boyfriend was in cardiac arrest and the patient hypotensive and bradycardic. They were both transported to the ED, where the boyfriend was pronounced dead. EMS saw bottles containing ammonia and bleach on the kitchen table, and assumed that the deceased was stabbed with a syringe containing bleach and ammonia. When speaking to the detectives, they noted that the ammonia was purple in color, and bleach was white and cloudy, making it unlikely to be the source of clear liquid noted in the syringe.

Past Medical History: Healthy.

Physical Exam: In the ED, the patient was intubated, BP 80s/50s, and HR40. Her physical examination was otherwise unremarkable. The physicians couldn't see the injection site.

Laboratory Data: Initial VBG-pH 6.97/pCO2 42/HCO3 56/BE 10, O2 sat 66% on 100% FIO2 vent, ABG-pH 7.08/pCO2 19/pO2 310/HCO3 6, O2 sat 99% on 100% FIO2 vent, lactate 20 mmol/L, cyanide 76 (reported 1 week later).

Clinical Course. Vasopressors included dopamine, epinephrine, dobutamine, neosynephrine, and vasopressin. 5 g of hydroxocobalamin was given ˜3 hr after admission (Hour 3), ABG-pH 6.76/pCO2 36/pO2 155/HCO3 5, Lactate 21.4 mmol/L, WBC 46, Hgb 13, Hct 43.8, platelets 164, Na 120, Bicarb 6, Cr 2.4, AST 700, ALT 200. ECG showed sinus bradycardia. She continued to have a significant metabolic acidemia with an elevated lactate. Hour 6 she received another 5 g hydroxocobalamin despite maximal supportive therapy and the patient died on Day 2. Detectives ultimately determined that the substance in the syringe and the cup from which the boyfriend drank contained cyanide.

Autopsy Findings: The postmortem revealed decomposition of most body organs.

Case 131. Acute fluoride ingestion: undoubtedly responsible.

Scenario/Substances: A 51-y/o healthy male who worked at a water treatment plant came to the ED stating he had ingested 3 tablespoons of sodium silicofluoride (98%) 1 hrs prior in a suicide attempt.

Past Medical History: Healthy.

Physical Exam: Normal appearing male; BP 175/94, HR 118, RR 20, T 36.3°C, O2 sat 98% on room air.

Laboratory Data: Ca 9.2 (8.2 corrected); K 4.2; acetaminophen and salicylate were not detected.

Clinical Course: The patient's only complaint in the ED was bladder pain. At 3 hrs post ingestion he became agitated, developed a widened QRS complex with sinus bradycardia and became hypotensive (BP 80/50). He was given IV fluids, insulin, kayexalate, furosemide, CaCl2 (via peripheral line), 1 amp of sodium bicarbonate and 1 amp D50W. The ECG reverted to normal sinus rhythm. During this time the patient had an episode of severe respiratory impairment with agonal respirations that resolved with an albuterol treatment and supplemental oxygen by nasal cannula. He continued to complain of stomach pain for which he received hydromorphone. At ˜5 hrs post ingestion, he became pulseless and was resuscitated with epinephrine, atropine and 2 amps of calcium chloride. The ECG showed a wide QRS with long PR interval and peaked T waves. ˜2 hrs later, he again widened his QRS complex and had VT, then bradycardia and again became pulseless. Resuscitation was unsuccessful and he expired ˜8 hrs after ingestion.

Autopsy findings: Not performed.

Case 133. Acute nitric acid, cocaine, clonazepam, morphine ingestion, unknown: undoubtedly responsible.

Scenario/Substances: A 53-y/o female came to the ED after intentional ingestion of 6–7 ounces of acid compound containing nitric acid, selenium and copper compounds; pH 0–1.

Past Medical History: Multiple suicide attempts including self-inflicted gunshot to head and medication overdoses; history of bipolar disorder, crack cocaine abuse, and alcoholism.

Physical Exam: Responsive, severe abdominal pain, throat irritation, hematemesis and asking staff to “just let her die”. BP 135/70, HR 84.

Laboratory Data: Hgb 18, Hct 55, PT 13.5, INR 1.3; clonazepam 21 ng/mL; acetaminophen, salicylate and ethanol not detected. Blood screen positive for cocaine.

Clinical Course: Upper endoscopy showed the gastrointestinal lining to be black; the patient was admitted to the ICU and received a proton pump inhibitor and sulcralfate with normal saline at 100 ml/h with morphine prn. Day 2: the patient had 2 cardiac arrests and expired during the second arrest.

Autopsy Findings: The findings revealed acid injuries to the upper trachea and stomach. Toxicology revealed parent cocaine in postmortem blood and vitreous fluid, as well as breakdown products in ante- and postmortem blood, consistent with acute cocaine use. Postmortem blood screen was positive for cocaine, clonazepam 3.2 ng/mL, UDS was positive for benzodiazepine and cocaine. The cause of death was complications of acid ingestion. The manner of death was ruled a suicide.

Case 134. Acute hydrofluoric acid ingestion: undoubtedly responsible.

Scenario/Substances: A 54-y/o male ingested about 1 oz of rust remover containing 1.92% hydrofluoric acid. Within 1 hr, he arrived at the ED with headache, nausea, abdominal pain and bloody emesis.

Past Medical History: Insomnia, hypertension, diabetes mellitus and hyperlipidemia.

Physical Exam: Male patient with headache, nausea, abdominal pain, bloody emesis; BP 138/88, HR 78, RR 18, T 36.7°C.

Laboratory Data: At 40 min post-ingestion: Ca 9.3, Mg 2, Cr 1.9; at 3 hrs post-ingestion: ABG-pH 7.06/pCO2 32.9/pO2 465; At 4.5 hrs post-ingestion: ABG-pH 7.26/pCO2 35/pO2 111; Ca 7.8, Cr 1.9; HCO3 16.3; At 6 hrs post-ingestion: Ca 5.1, Cr 1.9, Mg 1.0; At 10 hrs post-ingestion: ABG-pH 7.6/pCO2 23.6/pO2 272; Ca 9.8, Mg 2.9.

Clinical Course: Initially the patient was given oral calcium tablets in the ED, he had a cardiac arrest, was resuscitated with defibrillation, IV atropine, epinephrine, calcium and midazolam. He was transferred to the ICU and had several additional cardiac arrests and was given Mg and NaCO3 and hemodialysis. His family agreed that further care was futile, comfort measures were instituted and he expired ˜11 hrs post-ingestion.

Autopsy Findings: Not performed. The death summary listed the cause of death as VF cardiac arrest from severe hypocalcemia, hypomagnesiumemia and metabolic acidosis due to intentional ingestion of hydrofluoric acid.

Case 138. Acute cyanide ingestion: contributory.

Scenario/Substances: 57-y/o male was brought to ED following ingestion of an unknown substance in an apparent suicide attempt. The patient had greeted EMS at his home and was walking at the scene, but lost consciousness during transport. A suicide note was found at the scene.

Past Medical History: Cerebral aneurysms s/p surgical clipping, severe migraine headaches, opioid dependence, ethanol abuse, s/p orchiectomy from testicular gang-related trauma. Social history: worked as a goldsmith.

Physical Exam: Unresponsive, diaphoretic male. BP 141/87, HR 80. Pupils midrange and reactive.

Laboratory Data: ABG-pH 7.58/PCO2 14/O2 99; anion gap 31, lactate 16 mmol/L; acetaminophen, salicylate and ethanol not detected; UDS: positive for amphetamines, opiates, benzodiazepines and THC. CxR: reported as negative.

Clinical Course: No response observed after naloxone. Intubation performed for airway protection, head CT negative. Further history from family indicated that the patient had sent an email indicating he planned to commit suicide using cyanide salts which he had access to as a goldsmith. The patient had an unexplained anion gap metabolic academia with serum lactate 16 mmol/L. Blood for measurement of serum cyanide was drawn and hydroxocobalamin 5 g IV was administered. The metabolic acidemia improved and the patient started to become more arousable, requiring a propofol infusion for sedation. Repeat ABG-pH 7.39/PCO2 35/PO2 209; repeat lactate 3 mmol/L. Upon transfer to the ICU he was noted to be “beefy red” with “raspberry colored urine”. He had transient elevated bilirubin, AST and ALT following hydroxocobalamin. On Day 2 the patient suffered a myocardial infarction followed by a cerebrovascular accident on Day 3. He was also treated for ethanol and opioid withdrawal with benzodiazepines and opioids. He was successfully extubated on Day 7. He has right sided flaccid paralysis and was transferred to a neurological unit. The patient did not pass swallowing tests and was given tube feedings but expired on Day 20 from an aspiration pneumonia.

Autopsy Findings: Cause of death: Aspiration pneumonia, CVA and cyanide poisoning. Pre-hydroxocobalamin whole blood cyanide concentration: 4.7 mcg/mL. Manner of death: suicide.

Case 153. Acute hydrofluoric acid ingestion: undoubtedly responsible.

Scenario/Substances: A 2-y/o male ingested an unknown amount of rust remover and possibly another cleaner at the babysitters. The babysitter called the father who came and picked up the child an hour later when he found the child in obvious distress. The child was crying, had vomited, and quickly became unresponsive. EMS was called and found the child in arrest. There were no obvious burns apparent in the child's mouth. He was noted to be in and out of v-fib and asystole, was intubated, defibrillated, received multiple doses of epinephrine, atropine, sodium bicarbonate, and was transported to the ED. The police alleged that the babysitter's home was a meth lab.

Physical Exam: Apeneic, pulseless, abdomen distended, head/neck, pharynx clear, unresponsive, no motor responses, reflexes absent, no signs of trama, no rash, pupils fixed and dilated, cyanosis noted around nail beds and eyes.

Laboratory Data: Initial, Ca 8.2, pH 6.1, phosphorus 9.5

WBC 5.8, RBC 1.91, Hgb 5.4, HCT 17

VBG-pH/pCO2 77/pO2 22/HCO3 9/BE -24.1, vO2 sat 12%.

Clinical Course: In the ED CPR was continued and the patient received multiple boluses of calcium carbonate and additional sodium bicarbonate. He received insulin for hyperkalemia and glucose for hypoglycemia. External cardiac pacing was attempted without capture or perfusion. CPR was discontinued after > 2 hrs.

Autopsy Findings: Cause of death was the toxic effecs of hydrofluoric acid ingestion and secondary hemorrhagic gastritis. Toxicology findings postmortem included methamphetamine blood < 0.01 mg/L, methamphetamine hair 1174 pg/mg.

Case 173. Acute mineral oil ingestion, ingestion with aspiration: undoubtedly responsible.

Scenario/Substances: A 2-y/o girl y ingested baby oil while exploring her environment. Her mother estimated the dose at 5–10 mL. She immediately started coughing and choking. Child's home nurse spoke with her physician. After 2 hr the nurse called EMS. The child was transported to the ED on oxygen; she continued to have respiratory distress en route.

Past Medical History: Trisomy 21 (Down's Syndrome), pulmonary hypertension, reactive airway disease, congenital heart disease, and severe dysphagia/swallowing disorder. Because of this last problem, she'd been fed by a gastrotomy tube and kept NPO for most of her life. She'd had prior admissions for respiratory distress, including 2 episodes of aspiration pneumonia after having gotten into food or drink. At home she had a constant attendant nurse, and lived on 2 L oxygen by nasal cannula.

Physical Exam: In the ED: HR 172, BP 113/59, RR 54, afebrile, O2 sat 72% on 2 L O2, in severe respiratory distress with wheezing, coughing, and use of accessory muscles of respiration.

Laboratory Data: Initial radiograph showed bilateral diffuse infiltrates, worse on the left side. Initial serum pH 7.46, pCO2 38, pO2 45, anion gap 12.

Clinical Course: On arrival at the ED, she was placed on a 100% non-rebreather mask, and given a series of albuterol aerosols. She had no improvement in respiratory status, so was endotracheally intubated and placed on a ventilator with 100% oxygen. Respiratory failure progressed, and on Day 1 x-ray findings and respiratory function, and she was switched to an oscilatory ventilator. Anemia was treated with packed RBCs. A cardiac arrest was treated successfully with CPR via APLS, after which she was enrolled in a prospective 3 day trial of hypothermia for cardiac arrest. She was randomized to the hypothermia arm. After rewarming on Day 3, her pulmonary status remained dismal. She remained ventilator dependant, developed abdominal compartment syndrome Day 44, and died on Day 45.

Autopsy Findings: Based on an external examination, the county coroner ruled cause of death was sepsis, due to aspiration pneumonia.

Case 174. Acute-on-chronic, 1,1-difluoroethane inhalation/nasal: undoubtedly responsible.

Scenario/Substances: A 28-y/o female with a history of huffing was found dead in her bed. She was last heard from 2 days prior to finding her deceased. There were ˜150 cans of hairspray in her bedroom.

Past Medical History: Home medications were omeprazole and promethazine.

Autopsy Findings: Postmortem labs (blood): Negative for ethanol, amphetamines, barbiturates, benzodiazepines, cocaine metabolites, opiates, PCP, THC metabolite, methadone, and propoxyphene. Volatile organic compounds: 1,1-difluoroethane 25 mcg/mL. Negative for other VOCs. Cause of death was death due to huffing.

Case 185. Acute hydrogen sulfide inhalation: undoubtedly responsible.

Scenario/Substances: A 20 yo male stopped his car on the interstate, called police, and reported that he had poisonous chemicals in his car and intended to commit suicide. When police arrived they found a note taped to the window stating that the car contained hydrogen sulfide. The police secured the scene and called hazmat. It took > 2 hr for the team to arrive. The patient was removed from the car and decontaminated on scene with soap and water. He was unresponsive, tachypneic and tachycardic. He vomited X2 in the ambulance during transport to the ED. The chemicals found in the vehicle were calcium polysulfide and hydrochloric acid, the ingredients in an internet recipe for hydrogen sulfide.

Physical Exam: In the ED: HR 124, BP 125/63, RR 32, the patient was thrashing around, but lacked purposeful movements. He was sedated, intubated, and ventilated; O2 sat was 98% after intubation. He had burns on his feet and what appeared to be corneal burns. There were abrasions on his face around the left eye and chin, possibly incurred during extraction from vehicle.

Laboratory Data: ABG-pH 7.1/pCO2 45/pO2 14/HCO3 14/BE -15.5, Glu 328, K 2.8, UDS-negative. Serum acetaminophen, ethanol and salicylate not detected. CxR clear.

Clinical Course: The patient received 1 amp of bicarb and IV fluids with 20 meq of K. He was given amyl nitrite 0.3 amp X 2, sodium nitrite 300 mg, and sodium thiosulfate 12.5 g. He was transported by air to a tertiary facility where he was admitted to the burn unit. His acidemia worsened, he arrested, and resuscitation was not successful.

Autopsy Findings: No autopsy performed.

Case 226. Acute carbon monoxide inhalation/nasal: undoubtedly responsible.

Scenario/Substances: A 60-y/o female was found unresponsive, apneic, and pulseless in her home after a house fire was extinguished. There had been intense thick black smoke in the house. She was found in PEA and resuscitated in the field.

Past Medical History: Hypertension, diabetes, COPD, ischemic heart disease, anemia, cardiomyopathy, placement of an internal cardiac defibrillator, mitral valve disease, dyslipidemia, recurrent gastrointestinal bleeding, narcotic and benzodiazepine abuse, and medical noncompliance. Medications included: lorazepam, ipratropium and albuterol nebulizers, amiodarone, amitriptyline, acetylsalicylic acid, buspirone, carvedilol, furosemide, levothyroxine, lisinopril, omeprazole, potassium, quetiapine, spironolactone, warfarin, zolpidem, venlafaxine, and home oxygen therapy.

Physical Exam: Unresponsive, intubated female; BP 80, without spontaneous respirations. Atraumatic with fixed and dilated pupils. A large amount of soot was on her face and body. Skin: warm and dry, without burns or edema; Lungs: clear to auscultation; Heart: irregular rhythm; Abdomen was soft, nontender, and nondistended; GCS 3.

Laboratory Data: ABG-pH 7.29/pCO2 45/pO2 118; COHb 29%;

Lactate 7.5, AST 90, ALT 77, albumin 2.8, total protein 5.4; PT 18.4, INR 1.8, PTT 32.6; CK 110, CKMB 2.1, troponin 0.04, WBC 12.2, Hgb 9.0, platelets 306; acetaminophen 4.0 mcg/mL, salicylic acid 3.8 mg/dL, UDS negative for amphetamines, phencyclidine, barbiturates, benzodiazepines, cocaine, marijuana, opiates and methadone. Day 2 HCO3 13, AST 1551, ALT 1469, Alk phos 165; PT 41, INR 3.9, WBC 16.4, Hgb 11, platelets 236. ECG irregular rhythm with HR 71, QRS 182, QTc 535 with left bundle branch block, no acute ST elevations or depressions.

Clinical Course: The patient had several subsequent asystolic arrests requiring resuscitation. She was given one 50 mL vial of 25% sodium thiosulfate over 2 min and sodium nitrate (300 mg over 10 min). There was no improvement in neurologic status; T increased to 40.6°C with consolidation noted on chest x-ray. She underwent brain activity testing later in the day and expired ˜36 hrs after presentation.

Autopsy Findings: Moderate to severe atherosclerotic cardiovascular disease and evidence of bronchopneumonia and necrotizing bronchitis/bronchiolitis with focal sloughing of the respiratory epithelium and acute and chronic inflammation. Necrotizing inflammation present within the submucosa and mucosa of the trachea. Brain revealed eosinophilic degeneration of the neurons consistent with hypoxic damage. Cause of death: complications of thermal inhalational injuries from products of combustion with a significant contributing factor being ischemic heart disease. Toxicological analysis of premortem blood obtained at the time of admission did not detect ethanol.

Case 228. Acute methane inhalation/nasal: probably responsible.

Scenario/Substances: A 62-y/o male was working with others in a manhole, changing a valve, when his co-workers heard a pop and gas started to come out of the line. The patient, who was closest to the gas leak, collapsed immediately. EMS administered 3 doses of epinephrine and 2 doses of atropine.

Physical Exam: Unresponsive, pulseless male patient arrived in ED with CPR in progress. No external signs of trauma; skin: normal color, no unusual odors detected; abdomen: soft; extremities: no edema or cyanosis.

Laboratory Data: Glu 65; cardiac monitor: asystole. In the field: EMS reported fire department environmental oxygen levels were measured low at 10% and the methane level was 89%. Carbon monoxide was not detected.

Clinical Course: CPR/ACLS continued; the patient briefly had fine VF and was defibrillated twice. Subsequently he had short episodes of a detectable pulse but relapsed into a pulseless state. Transcutaneous cardiac pacing was attempted unsuccessfully. Resuscitation efforts were terminated after ˜1 hr.

Autopsy Findings: Rib fractures consistent with CPR were evident; no discoloration of organs or tissues was noted. Cause of death: secondary to complications from exposure to a noxious gas, presumably methane. Subsequent investigation of the worksite indicated rising levels of inflammable gases although the test could not distinguish between methane and propane. No methane or ethanol was detected in postmortem aortic and femoral blood samples, respectively.

Case 252. Thallium ingestion: undoubtedly responsible.

Scenario/Substances: A 39 yo male software engineer drove himself to the ED, and stated that he thought someone was poisoning him. He reported acute onset abdominal pain 1–2 hr after eating lunch of homemade rice and green beans. He reported nausea without vomiting, dull abdominal pain progressing in intensity, and non-bloody diarrhea. His wife ingested the same food, reported diarrhea but no pain. She reported that their child was recently hospitalized with a similar illness.

Past Medical History: His past medical history was unremarkable. Social history obtained 4 days after admission revealed that the husband and wife had filed for divorce in the previous year and the court date was the day of ED admission. His wife was a chemist and he suspected that she might be poisoning him.

Physical Exam: In the ED, the readings were HR 63, BP 137/89, RR 20. Physical exam was unremarkable including his abdominal exam.

Laboratory Data: Normal CBC, electrolytes, and liver functions. Abdominal ultrasound and CT of the abdomen and pelvis were unremarkable.

Clinical Course: Later on the day of admission, he began complaining of hyposthesias (pins and needles) and bilateral parasthesias of his hands, and then a day later developed painful paresthesias of his feet. These parasthesias progressed during the hospital stay as did his abdominal pain. Eventually the paresthesias became so severe that he could not move his legs. He reported an episode of paresthesias a year earlier and that this episode had started 2 days before admission. Guillain Barre Syndrome was suspected and he received IV immunoglobulin with no relief of symptomatology. He developed fluctuating levels of alertness and on Day 8 day he was found actively seizing, required large doses of anti-convulsive medication, became ventilator dependent, and was transferred to the ICU. On Day 10, a 24 hr urine for heavy metal screen was reported negative for lead, mercury. On Day 12 a 24 hr urine for thallium level was reported as > 800 mcg/L on a 4300 mL urine volume. On Day 12, he developed hypotension, received pressor support, multiple dose activated charcoal every 4 hrs, 2 g Prussian Blue, and high flux hemodialysis. Medicinal grade Prussian Blue was unavailable, so the patient received technical grade reagent. Despite aggressive therapy he developed 2 episodes of PEA and could not be resuscitated from the second, and died on Day 12.

Autopsy Findings: Embargoed by prosecutor's office.

Case 262. Acute fluorinated hydrocarbon inhalation: undoubtedly responsible.

Scenario/Substances: A 22-y/o female presented to the ED with cardiac arrest after reportedly huffing a cleaning product that contained difluoroethane. She was endotracheally intubated by EMS prior to arrival.

Past Medical History: Methamphetamine use.

Physical Exam: Patient was comatose. She was successfully resusciated (atropine, IVFs and CPR) with initial BP 130/100, HR 152, RR 20 (ventilated). O2 sat 90% on 100% FiO2.

Clinical Course: Patient was resuscitated with return of spontaneous circulation and was sedated and ventilated. Head CT showed a diffuse intracerebral bleed with subsequent edema. CxR suggested aspiration. The initial use of epineprhine was withheld due to concern about potential hydrocarbon-induced myocardial sensitization. She was taken to the operating room to evacuate the clot, but suffered a cardiac arrest and was instead returned to the ICU. She was cardioverted for VF and started on vasopressors for hypotension but died from a cardiac arrest within 24 hr of admission.

Autopsy Findings: Bilateral pleural effusions. Blood and bile positive for 1,1 diflouroethane.

Case 267. Acute fluorinated hydrocarbon inhalation: undoubtedly responsible.

Scenario/Substances: A 25-y/o male was found apenic by his roommate (last seen 4 hrs earlier). The roommate called 911 and began CPR. EMS found the patient cold, cyanotic, and in asystole. They continued CPR, intubated him, and gave glucose, atropine, naloxone and epinephrine. A container of computer dusting solution containing difluoroethane was found near the patient.

Past Medical History: No known medical problems or regular medications.

Physical Exam: In the ED he was unresponsive, in asystole, T 34.3°C, pupils fixed and dilated.

Laboratory Data: Glu 183, bedside ultrasound showed no cardiac activity.

Clinical Course: ACLS CPR was continued and he was given IV saline and bicarbonate without response and he was pronounced dead.

Autopsy Findings: Gross and microscopic examinations were unremarkable. The heart was 310 gm and showed no abnormalities of the coronary or great vessels, no focal wall or valvular defects, and no focal areas of discoloration, softening or scarring. Difluoroethane concentrations: iliac blood 1.64 mg/L, urine 3.54 mg/L, vitreous humor 0.97 mg/L. The cause of death was determined to be difluoroethane intoxication.

Case 281. Acute lamp oil ingestion and aspiration: undoubtedly responsible.

Scenario/Substances: A 22 m/o female ingested and aspirated tiki torch fuel, a hydrocarbon, and began to cough. She was transported to the local ED.

Physical Exam: Coughing toddler in significant respiratory distress; hypotensive, with frothy, bloody secretions.

Laboratory Data: ABG-pH ‘acidotic, not recordable’ pCO2 248/pO2 33, K 8, Glu 700, lactate 12. CxR: R lung “white out”.

Clinical Course: The patient was suctioned and returned bloody and frothy secretions prior to being intubated, ventilated and transferred to a tertiary care facility able to provide a higher level of care. Upon arrival, she experienced a cardiac arrest from which she could not be resuscitated. The patient expired within 1 hr after ingestion.

Autopsy Findings: Cause of death; chemical pneumonitis due to hydrocarbon toxicity. Lungs: microscopic exam revealed extensive alveolar wall damage, neutrophilic and eosinophilic infiltrate, acute hemorrhage and extensive edema fluid; Heart: microscopic exam revealed a focal area of lymphocytic infiltrate with myocyte necrosis with a few histocytes and eosinophils. Focal myocarditis was determined although thought not be associated with hydrocarbon ingestion per the ME report. The myocarditis was focal and determined as most likely not contributing to cause of death. Antemortem blood specimen did not detect solvents or volatiles.

Case 283. Acute cyclopeptide mushrooms ingestion: probably responsible.

Scenario/Substances: A 70-y/o female with an extensive medical history presented to the ED with nausea, vomiting, and diarrhea ˜10 hr after a meal she made with small brown mushrooms that were picked from her brother's back yard.

Past Medical History: Colon perforation with partial bowel resection, anemia, systemic lupus erythematosis, emphysema, osteoporosis, cerebrovascular accident, acute myocardial infarction, hypothyroidism, gastroesophageal bleeding, pneumonia.

Physical Exam: Awake and cooperative, and at her baseline speech and mentation, BP 138/80, HR 82, T 36.6°C, RR 15, O2 Sat 95%, no jaundice or liver tenderness.

Laboratory Data: AST 108, ALT 69, INR 1.04, lipase 30.

Clinical Course: The patient was started on IV normal saline, ondansetron to control nausea and vomiting, and oral activated charcoal. Cyclopeptide mushroom poisoning was suspected and serial liver function tests were performed. The mushroom was not positively identified but a mycologist who looked at a digital photograph of leftover mushroom segments opined it was consistent with galerina spp. She received further doses of activated charcoal, and was started on IV N-acetylcysteine and cimetidine. Day 2 AST 810, ALT 577, INR 1.91. Her clinical status abruptly deteriorated, with hypoglycemia and metabolic acidosis, and she was intubated. She developed a fever of 39.1°C. She also developed acute renal failure, and hypotension requiring norepinephrine. Her urine and blood cultures were positive for E. coli. The investigational drug silibinin was obtained and started IV on Day 2. However, she did not improve, and Day 3 readings were AST 1297, ALT 1365, INR 6.58, lactate 6.7 mmol/L. Based on the prognosis, the family opted for institution of comfort measures and she expired shortly thereafter.

Autopsy Findings: No autopsy was done. The coroner reviewed the case and determined that the cause of death was acute hepatic failure due to Amanita mushroom poisoning (although Galerina spp. seems more likely).

Case 295. Acute malathion ingestion: undoubtedly responsible.

Scenario/Substances: A 57-y/o female was seen by her family ingesting 50% malathion liquid in a suicide attempt. The family called EMS. The patient had progressive neurologic decline en route to the hospital, she vomited and then became unresponsive on arrival to the hospital with possible seizure activity. She was given 2 mg of atropine by EMS. The bottle of malathion brought to the hospital was empty and was found to contain 50% malathion (unknown quantity ingested).

Past Medical History: Previous suicide attempts, ethanol abuse.

Physical Exam: HR 135, BP 123/60, RR 16 and labored. Skin warm and diaphoretic, Thick oral secretions, pupils 5 mm and not reactive, scattered rhonchi, bowel sounds increased. She was unresponsive, GCS 3, normal muscle tone, no seizure activity.

Laboratory Data: Calcium, 8.4, magnesium 1.8

phosphorus 1.6, lactate 6.8 mmol/L, AST 21, ALT 11, PT 13.1, PTT 26.6, acetaminophen 7 ug/ml, salicylate not detected. On Day 2 RBC acetylcholinesterase 8.6 U/gHb pseudocholinesterase not detectable.

Clinical Course: On her arrive at the ED she was intubated and decontaminated and given pradlidoxime IV. She was started on midazolam and fentanyl for sedation. She was kept on midazolam 10 mg/hr for seizure prophylaxis with continuous EEG monitoring. No seizure activity was noted, and on Day 2 she was weaned from midazolam. She was treated with pralidoxime at 500 mg/hr for 48 hrs followed by 250 mg/hr thereafter. Urine output was 12 L on Day 1, 7 L on Day 2, replaced with normal saline. Her hypotension required norepinephrine on Day 1 + vasopressin, phenylephrine and later dopamine on Day 2. Based on the prognosis, the family opted for institution of comfort measures and she expired on Day 3.

Autopsy Findings: Not performed.

Case 304. Acute ibogaine ingestion: undoubtedly responsible.

Scenario/Substances: 25-y/o ingested 2 gm of ibogaine he purchased through the internet for treatment of opiate dependence. The patient was suffereing from cardiac arrest when EMS arrived. According to the patient's AICD, the cardiac arrest was Vtach/Vfib.

Past Medical History: heroin abuse, SVT, AICD-pacemaker

Physical Exam: BP 113/111, HR 120, RR 12, pupils dilated, bowel sounds present, skin warm and dry, comatose, deep tendon reflexes intact without hyperreflexia.

Laboratory Data: Ca 10.7, phos 9.3, Mg 2.4, lactate 18.

Troponin 0.33 ng/ml, Hb 13.3, platelets 139, WBC 21, INR 1.33, ECG: QRS 208, QTc 521, Rate 112. EEG showed seizure activity and early encephalopathy.

Clinical Course: Patient was resuscitated and started on norepinephrine, phenylephrine, bicarbonate, and amiodarone. He remained hyperthermic and hypotensive despite multiple vasopressors. His lactic acidosis initially improved, but he developed hypotension, acidosis, and multisystem organ failure on Day 2. His anion gap increased to 20 with an ABG pH 7.2, ALT 491, AST 1099. The patient's EF was 10% on echo. Intralipid and balloon pump were discussed but the patient had no signs of brain activity, comfort measures were instituted and he expired on Day 2.

Autopsy Findings: Ibogaine in the heart blood 2.2 mcg/ml, iliac blood 1.8 mcg/ml, vitreous 0.98 mcg/ml, and liver 4.2 mcg/g. Along with the patient's pre-existing heart condition, ibogaine was determined to be the cause of death. Samples of the capsules were obtained and tested via GC MS – only ibogaine was found. The 3 capsules tested had significantly different amounts of ibogaine in them so it is difficult to know how much was actually ingested.

Case 305. Acute aconite, ethanol ingestion, dermal: undoubtedly responsible.

Scenario/Substances: A 28-y/o male contacted EMS to report trouble breathing. EMS found him vomiting, agitated and complaining of chest pain, and feeling as if limbs were paralyzed. He indicated that he ingested a poisonous plant by pointing at the label from a recently purchased nursery plant that read: Aconitum, Blue Lagoon, Monkshood. During transport, he developed VT then VF.

Past Medical History: Social history: patient's father committed suicide a few months prior to this event.

Physical Exam: Tachycardia with shallow respirations.

Clinical Course: Unresponsive male in ED with VF during transport to the ED. He was intubated and defibrillated into sinus rhythm briefly before developing torsade de pointes from which he could not be resuscitated. He expired in the ED.

Autopsy Findings: Severe pulmonary congestion, normal heart examination. The deceased was in possession of Monkshood and Delphinium plants and had knowledge of the poisonous nature of the plants from the sales persons at 2 local nurseries and recent internet searches found on his personal computer. At the scene, personal and financial papers were prominently displayed including an internet-purchased will. The manner of death was suicide.

Case 308. Acute methadone ingestion: undoubtedly responsible

Scenario/Substances: A 2-y/o girl drank juice then complained that her tongue “felt weird”. She then took a nap and was found cold, limp and barely breathing. It was later discovered the juice had been mixed with methadone.

Physical Exam: Unresponsive, bradycardic, hypotensive 2-y/o female with cold extremities.

Clinical Course: No response was noted to naloxone administration. Patient was intubated and placed on a naloxone infusion. Urine toxicology was not tested for methadone. The patient was transferred to a tertiary care center where urine toxicology was positive for methadone. The family repeatedly denied presence of any methadone in the household. In the pediatric ICU, urine also positive for methadone. Day 2 CT scan of head showed cerebral edema with herniation. Naloxone was discontinued after 48 hrs. Serum samples were sent out for quantification of methadone. The patient was declared brain dead on the Day 6 and expired on Day 7.

Autopsy Findings: Premortem blood methadone concentrations: 219 ng/mL at 24 hrs, and 178 ng/ at 48 hrs. CNS: cerebral edema with severe diastatic separation of cranial sutures; acute hypoxic/ischemic encephalopathy, secondary subarachnoid hemorrhage of right occipital and bilateral temporal lobes. Secondary autolysis of brain parenchyma. Lungs, spleen, liver, adrenal glands, large vessels, and kidneys were procured for organ donation. Cardiovascular system: normal. Cause of death: Methadone intoxication. Manner of death: Could not be determined.

Case 311. Acute methadone ingestion: undoubtedly responsible.

Scenario/Substances: 9-y/o boy had difficulty falling asleep and, because the family ran out of diphenhydramine, ingested his mother's methadone (50 mg, liquid). Patient did not wake up for school at 5 hrs later. EMS found him suffering from cardiac arrest. Naloxone was administered with no response. CPR was initiated; the patient was intubated and transported to the ED.

Past Medical History: Obesity.

Physical Exam: Intubated male in full cardiac arrest.

Laboratory Data: ABG-pH 6.97/pCO2 66/pO2 109/HCO3 14; UDS positive for methadone.

Clinical Course: Additional naloxone was administered for a total of 4 doses with no response. Multiple doses of epinephrine were given with return of spontaneous circulation after 1 hr and the patient was admitted to the ICU where he remained comatose and exhibited post-anoxic myoclonus. Day 2 he developed diabetes insipidus. Brain perfusion studies were negative; thrombocytopenia occurred and the patient had bleeding from the nose and mouth. The urine toxicology remained positive for methadone for a total of 7 days. The patient was declared brain dead; comfort measures were instituted on Day 8, the patient expired on Day 10.

Autopsy Findings: Liquification of the majority of the brain with small hemorrhagic infarctions in lungs; myocardium was normal with no infarction. Cause of death: Methadone Intoxication. Manner of death: “could not be determined”.

Case 324. Acute methadone ingestion: undoubtedly responsible.

Scenario/Substances: A 17 year old male self-medicated with his grandmother's methadone for pain after playing in a football game. He had started to slur his words, but drove himself home. He was found the following morning after last being seen at ˜2AM; EMS found him unresponsive and asystolic. CPR was performed and circulation restored. Naloxone was given without response.

Past Medical History: Broken arm, depression, asthma

Physical Exam: BP 132/88, HR 125, RR 24 (on ventilator), T 33.1°C.

Laboratory Data: Ca 5.8, Mg 1.9, phos 10.6; Hgb 16, Hct 45,.

methemoglobin 1.1%, COHb 2.1%; PT 19.5, PTT 35.2, INR 1.7; AST 5428, ALT 5840. UDS: negative × 2 and positive × 1 for methadone; acetaminophen, salicylate and ethanol not detected.

Clinical Course: Head CT showed diffuse cerebral and cerebellar edema with no acute hemorrhage or masses. He was maintained on a ventilator and was given metaraminol and epinephrine, later switched to dopamine and epinephrine for hemodynamic support. He was able to breath when ventilator support was temporarily decreased but showed no other positive neurological signs; pupils were fixed and dilated, no pain or gag reflexes were present. Day 2, comfort measures were instituted and the patient expired.

Autopsy findings: Premortem lab results revealed methadone, 420 ng/mL; EDDP 483 ng/mL; escitalopram was not detected. The results were consistent with death secondary to methadone toxicity. The negative escitalopram level suggested that he was non-compliant with his antidepressant medication.

Case 816. Acute acetaminophen ingestion: undoubtedly responsible.

Scenario/Substances: A 48-y/o female was transferred to a tertiary care hospital for consideration of liver transplantation after an acetaminophen overdose.

Past Medical History: Depression, prior suicide attempt by acetaminophen overdose, cesarean section, ankle surgery.

Physical Exam: Upon arrival to the tertiary care facility the readings were HR 139, BP 139/61, T 36.6°C, O2 sat 100% on 100% FiO2. She was minimally responsive to verbal stimuli. Liver edge was palpable approximately 2 cm below the right costal margin. Examination otherwise unremarkable.

Laboratory Data: Acetaminophen at the first hospital was 77 mg/L (time not known, this was 2 days before transfer to tertiary care). On arrival at the tertiary care hospital, acetaminophen was < 10 mg/L, ALT 8,000, AST 16,000, serum pH 7.24, ammonia 37 umol/L.

Clinical Course: Prior to transfer to tertiary care, she had received oral n-acetylcysteine. On arrival at tertiary care center, she was switched over to IV n-acetylcysteine, 6.25 mg/kg/hr. Hemodiafiltration was performed. On that same day, she was given sedation and endotracheally intubated. She was given oxygen via the endotracheal tube and ventilator. On Day 2 she was more alert; n-acetylcysteine dosing was adjusted based on patient weight. On Day 3 AST 3800, ALT 3600, INR 3 platelets 37. FFP and antibiotics were given. The patient developed atrial fibrillation with a ventricular rate of 125 and stable BP 94/54. On Day 4, her readings were AST 600, ALT 2,000, INR 2.2 total bilirubin (total, 6.2; direct 3.7), N-acetylcysteine was continued. On Day 6, CNS depression increased, total bilirubin 7, AST 200; ALT 1200. N-acetylcysteine treatment was discontinued. Over the next 10 days, the patient's clincal status fluctuated, her transaminases decreased and her bilirubin increased. She became hemodynamically unstable. Based on the prognosis, the family opted for institution of comfort measures and he expired on Day 18.

Autopsy Findings: Coroner's report identified immediate cause of death to be widespread hepatic necrosis as a consequence of acute intoxication by acetaminophen. Manner of death was suicide. Other significant conditions included renal tubular necrosis, ascites, bilateral pleural effusions, pulmonary edema, and cerebral edema.

Case 1151. Acute buprenorphine and naloxone ingestion: undoubtedly responsible.

Scenario/Substances: A 13 month old male was found unresponsive in his crib after a suspected exposure to buprenorphine and naloxone sublingual film.

Clinical Course: The evening before admission, the parents gave the child a bottle of buprenorphine and naloxone as a rattle. The parents later noticed that the bottle was opened and the patient had several pill fragments in his mouth and they removed them. Subsequently, the patient was fed and laid to sleep. The following morning, the child was found unresponsive by the parents and EMS was summoned. At the scene, the patient was reported to be in cardiopulmonary arrest, resuscitation was initiated and 0.8 mg of naloxone was administered without any response. The patient was declared dead on arrival to the ED. Child protective services and the ME were notified.

Autopsy Findings: The cause of death was determined to be acute buprenorphine intoxication. The patient's blood levels were buprenorphine 52 ng/ml, norbuprenorphine 23 ng/mL, and naloxone 39 ng/mL. Gastric contents buprenorphine was 7400 ng/mL, norbuprenorphine 84 ng/mL, and naloxone 970 ng/mL.

Case 1161. Acute bupivacaine injection: undoubtedly responsible.

Scenario/Substances: 50-y/o. male was having knee arthroscopy at a surgery center using a nerve block. Bupivicaine 0.5%, 30 ml was infiltrated. During administration the patient had an asystolic cardiac arrest. Fentanyl and midazolam had been given prior to the bupivicaine. CPR was immediately started.

Past Medical History: Diabetes.

Physical Exam: Unresponsive male: CPR in progress. No signs of trauma, pupils: fixed and dilated, absent corneal reflex.

Laboratory Data: ABG-pH 6.85/pCO2 92/pO2 24/HCO3 16;

AST 422, ALT 413, Alk phos 81, Osmol 255, WBC 7.5, Hgb 11.9, Hct 39.9, Ca ionized 1.05, Ca 7,2, tot protein 4.4, albumin 2.3, tot bilirubin 0.42, CKMB < 1, myoglobin 362, troponin < 0.05.

Clinical Course: CPR/ACLS was immediately instituted with endotracheal intubation, epinephrine ×3, vasopressin ×3, atropine, dopamine, and 2 doses of 250 ml of intralipid. The patient was transferred from the surgery center to the ED. Right main stem intubation was corrected by ETT repositioning. Procainamide was given, followed by a third bolus of intralipid (20% 1.5 ml/kg) then by constant IV infusion at 0.25 ml/kg. Multiple doses of sodium bicarbonate, CaCl2, calcium gluconate, epinephrine, infusions of dopamine, intralipid and a total of 9L of IV fluids. External pacing was attempted multiple times without success. Resuscitation efforts were terminated after 4 hrs with continued, refractory asystole.

Autopsy Findings: Not available.

Case 1169. Chronic, thrombin inhibitor ingestion: undoubtedly responsible.

Scenario/Substances: A 74-y/o female with an extensive cardiac history, being treated with dabigatran for atrial fibrillation, was referred by her PCP for anemia, acute renal failure, and coagulopathy. On presentation, she reported 1 day of increasing weakness and tremor in addition to black stools for the last 4 days.

Past Medical History: Ischemic cardiomyopathy with EF 30–35%, previous coronary stent, prior PEA arrest, with AICD, mitral valve repair, severe pulmonary hypertension, chronic atrial fibrillation. Medications: torsemide, digoxin, metoprolol (sustained release), colchicine, salicylate, simvastatin, dabigatran, clonazepam, omeprazole, nitroglycerin SL.

Physical Exam: In the ED: HR 90, BP 88/44, T 36.3°C, RR 19, O2 sat 99% on room air. She appeared chronically ill and borderline cachectic, but alert and oriented. Chest clear, heart sounds irregular (a fib), abdomen soft, trace extremity edema. NG lavage with minimal blood, guaiac positive with frank melena.

Laboratory Data: In the ED.

Hgb 9.2, Hct 27.1, WBC 7.6, platelets 98, INR > 13.7, PTT > 100, AST 44, ALT 30, alk phos 72, T-Bili 1.4, CxR: no consolidation or pulmonary edema, EKG: atrial fibrillation, old Q waves in III, aVF

Clinical Course: The patient received 1 L of crystalloid fluids gently and was transferred to the ICU. No blood products were given initially. On Day 2, she was started on CVVHD to facilitate dabigatran clearance. Shortly thereafter she went into pulseless VT that decompensated into PEA arrest with return of spontaneous circulation after CPR/ACLS. Throughout her hospitalization the patient developed progressive, worsening abdominal pain, hematemesis, melena, and infective colitis. She received vitamin K, desmopressin, and multiple units of packed RBC, FFP, platelets, and PCC. She required multiple vasopressors to maintain her BP. Despite these efforts, she died on Day 7.

Dabigatran Concentrations: Dabigatran from serial serum samples obtained during CVVHD were: > 500 ng/mL at 3 and 6 hr and 225 and < 45 ng/mL (pre- and post-filter) at 23 hr. One dialysate sample was > 800 ng/mL. Reported concentrations at steady state in patients taking a dose of 220 mg daily ranged from 64 to 443 with a mean of 184 ng/mL.

Autopsy Findings: Not performed.

Case 1170. Acute clopidogrel, salicylate, dabigatran ingestion: undoubtedly responsible.

Scenario/Substances: A 79-y/o male presented with epistaxis and melena.

Past Medical History: Atrial fibrillation, CAD s/p CABG, on aspirin 81 mg, Plavix, and dagibatran 150 mg bid

Physical Exam: BP 83/52, HR 88, RR 17, O2 sat 97%. Copious bleeding from nose, both anterior and posterior, no neuurological deficits.

Laboratory Data: Hgb 4.9, platelets 278, INR 1.9, PTT 96.9

AST 58, ALT 22.

Clinical Course: The patient was intubated shortly after arrival for airway protection, and nasal packing was placed, but he continued to bleed around the packing. He was given FFP, packed RBCs, platelets, cryoprecipitate, and desmopressin. He was started on levophed and dopamine for hypotension. Over the course of Day 1, he had ongoing bleeding, hypotension, and evidence of tissue hypoperfusion. Lactate was 5.8, troponin was initially 2.85 and peaked at 13.

Hgb was 8.1 after multiple transfusions, platelets 141 after 4 units, AST 1000, ALT 611, INR 5.8 to 3 after vitamin K.

He received a total of 18 units FFP, 4 units platelets, 20 units cryoprecipitate, 12 units RBCs, 2 doses of desmopressin, and 3000 units of prothrombin complex concentrate. Early in Day 2 he was noted to have copious bleeding form nose and rectum. In the afternoon he became bradycardic to 40s, CPR was initiated. Based on the prognosis the family opted for institution of comfort measures and he expired early on Day 3.

Autopsy Findings: Not performed.

Case 1235. Unknown, ethanol, amitriptyline, cocaine, gabapentin ingestion: undoubtedly responsible.

Scenario/Substances: A 40y/o, 65 kg male was found unresponsive in his home by his family. He was found next to an empty bottle of amitriptyline 8 hrs after he was last seen “normal” but drinking alcohol. The suspected ingestion was up to 3 g of amitriptyline with unknown amounts of ethanol throughout the night.

Past Medical History: Depression, ethanol, caffeine, tobacco and recreational drug abuse. Routine medications were unknown.

Physical Exam: Unresponsive male; BP 92/60, HR 132.

Laboratory Data: ABG-pH 7.2/pCO2 63.7/pO2 429; O2 sat 100% after intubation and mechanical ventilation;

Ca 8.0, Mg 2.2, CK 428, myoglobin 557 ng/mL, CK MB 5.4 ng/mL; Hct 43; ECG: rate 165, QRS 156, QTc 596. UDS positive for cocaine, negative for barbiturates, benzodiazepines, methadone, opiates, phencyclodine, and marijuana; acetaminophen. Serum salicylate and ethanol not detected. CT scan of the brain and chest x-ray reported as “negative”. The QRS remained elevated (129, 130, 136, 140 and 122) for 9, 15, 24, 38 and 40 hrs post admission. The QTc intervals varied from 472 to 596 (562 at 48 hrs post admission) over the same time period.

Clinical Course: In the ED, the patient was given 3 doses of sodium bicarbonate (50 mEq each) for a widened QRS with no improvement then 100 mg of lidocaine IV and placed on a lidocaine infusion for ventricular tachycardia after 3 unsuccessful attempts with cardioversion. At 4 hrs, when VT resolved, lidocaine was discontinued and he was transferred to a tertiary HCF. There he was treated with thiamine, multivitamin, enoxaparin, famotidine, as well as lorazepam prn for agitation and morphine prn for pain. At 36 hrs post admission he demonstrated intermittent myoclonic jerking followed by a seizure after an EEG was completed, which resolved spontaneously. 3 hrs later, a second seizure occurred and he was treated with IV lorazepam 5 mg just prior to a cardiopulmonary arrest from which he could not be resuscitated. The patient expired ˜40 hrs after he arrived to the initial HCF.

Autopsy Findings: Not performed. ME report listed the cause of death as amitriptyline toxicity with cocaine contributing to patient's death. Antemortem blood testing from the initial HCF showed blood amitriptyline 2.1 mg/kg, nortriptyline was not detected benzoylecgonine 0.044 mg/L, gabapentin 15 mg/L and presence of benzodiazepines, midazolam and lidocaine. Cocaethylene, cocaine, ethanol, opiates and opioids were not detected. The concentrations of amitriptyline and benzoylecgonine were found in amounts consistent with those previously reported in fatal cases.

Case 1238. Acute-on-chronic, bupropion, and ethano ingestion: undoubtedly responsible.

Scenario/Substances: This 40-y/o female was brought to ED after being stopped by police for erratic driving. Police noted altered mental status, and she told the police officer she had taken an overdose. An unidentified white powder was found in her car.

Past Medical History: Medications included bupropion and acamprosate.

Physical Exam: HR 110, BP 70/40. Pupils 4 mm and reactive. Oral mucosa dry with white chalky material around mouth. EKG sinus tachycardia with QRS 98 and QTc 470.

Laboratory Data: ABG-pH 7.23/pCO2 41/pO2 371/HCO3 18; 1 hr later ABG-pH 7.14/pCO2 38/pO2 136/HCO3 14.

Anion gap 19, lactate 8.1, CK 126, ammonia 82, acetaminophen and salicylate was not detected, ethanol 307 mg/dL, UDS positive for amphetamines and benzodiazepines.

Clinical Course: In ED, her mental status continued to deteriorate; she became unresponsive to painful stimuli, then had 3 tonic-clonic seizures. BP 50/30. She was intubated and sedated with propofol. Lorazepam and phenytoin were given for seizure activity and norepinephrine was started. Lipid emulsion given and sodium bicarbonate infusion was begun. In ICU T 38.9°C, HR 120s, she received phenylephrine and vasopressin in addition to norepinephrine to maintain BP Midazolam was given for continued seizures, T increased to 40 despite external cooling. Pacing was initiated and dopamine and epinephrine were added. She experienced PEA and asystole, which failed to respond to ACLS resuscitation and she died ˜14 hr after presentation to ED.

Autopsy Findings: Autopsy revealed fatty liver with severe mixed micro- and macrovesicular steatosis (fatty change). Despite postmortem bupropion levels lower than those reported in bupropion fatalities, her very elevated hydroxybupropion and her clinical picture of coma, seizures, and metabolic acidosis were judged consistent with bupropion toxicity. Cause of death was bupropion toxicity, and manner of death was accident.

Case 1276. Acute amitriptyline ingestion: undoubtedly responsible.

Scenario/Substances: A 48 y/o woman, discharged from prison earlier that day took an unknown number of amitriptyline pills while in the car with her husband. She vomited with several undigested pills in the emesis, became unresponsive, and her husband started CPR and called EMS.

Past Medical History: Bipolar disorder, seizures, and cerebral aneurysm. Medications included amitriptyline, sertraline, and oxcarbazepine.

Physical Exam: Unresponsive patient in cardiac arrest with seizure activity.

Laboratory Data: Cardiac monitor: wide complex tachycardia similar to VT; toxicology screen detected THC, cocaine and tricyclic antidepressants.

Clinical Course: The patient received multiple doses of diazepam and was defibrillated without effect. Transfer to another hospital by air occurred during which time 1 amp of NaHCO3 was given. Four hours after arrival at the second HCF, hypotension continued, the QRS was 276 and she was defibrillated and given lidocaine, and 2 amps of NaHCO3, which resulted in a QRS of 148. Bicarbonate and norepinephrine infusions were initiated. Lab data: pH 7.37,

At 7 hrs, VT occurred treated with K, NaHCO3 and Mg. VS improved to BP 124/73, HR 106, RR 10 with O2 sat 99% on FIO2 0.50. IV fat emulsion, lidocaine, and insulin were added therapeutically. Further lab data showed:

PO4 0.5, Mg 1.7, and ionized Ca 0.92. Seizures recurred at 19 hrs post ingestion, treated with 6 mg lorezepam successfully. Hypotension recurred, treated with NaCO3. Na was 174; pH 7.75. IV lidocaine and bicarbonate drips were stopped; vasopressin was added to the norepinephrine; BP 105/60, QRS 116 and QT/QTc > 500 ec. Multiple vasopressors were needed, aspiration pneumonia was suspected due to fever; On Day 2, she had PEA arrest from which she was resuscitated. On Day 3, pupils were 5 mm, with BP systolic 80. pH 7.69, pCO2 39, pO2 126, AST 1,131, ALT 1,150.

Comfort measures were put in place and the patient expired on Day 3.

Autopsy Findings: Not done. Cause of death: amitriptyline toxicity.

Case 1278. Acute venlafaxine ingestion: undoubtedly responsible.

Scenario/Substances: A 49-y/o male who was found down at home after ingesting an unknown number of 75 mg venlafaxine. The patient was lethargic with stable vital signs.

Past Medical History: Hypertension, hyperlipidemia, anxiety, depression, and prior suicide attempts × 3. Medications: simvastatin, lithium, risperidone, mirtazapine, venlafaxine, trazodone, losartan.

Physical Exam: HR, BP 127/66, T 37.1°C, RR 16–28, O2 sat 98–100% on 2 L nasal O2, somnolent but arousable, responding appropriately, exam otherwise unremarkable.

Laboratory Data: WBC 11.6, Hgb 14.3, Hct 42.4,

platelets 201, INR 0.9, PTT 22.4, AST 140, ALT 426, alk phos 190, T-bili 1.1, Ca 9.9, iCa 1.3, Mg 2.3, phos 2.7., serum osm 303, ABG-ph 7.25, ECG sinus tachycardia, QRS 106, QTc 396, serum acetaminophen, and salicylate not detected, Li 0.7.

Clinical Course: Several hours later he was more awake and additional history was obtained that he ingested up to 400 pills of venlafaxine extended release. HR at this time was 103, QRS 103. Aggressive gut decontamination was instituted with activated charcoal 50 gm every 2 hr for 4 doses and whole bowel irrigation. Later that day, his mental status deteriorated and he had 3 seizures that lasted about 15 s each, treated with lorazepam. He became hemodynamically unstable with QRS 134, BP 80/50 treated with IV fluids, sodium bicarbonate and norepinephrine. He was intubated and started on a propofol drip, and admitted to the ICU. He received multiple boluses of sodium bicarbonate for widened QRS and norepinephrine for hypotension. Whole bowel irrigation and charcoal had to be discontinued because the patient developed an ileus. The patient was treated with N-acetylcysteine for possible late acetaminophen presentation with transaminitis. Day 2 the QRS widened to 150, despite bicarbonate boluses. His Na was 158, pH > 7.5. He was treated with 2 boluses of intralipid, lidocaine, electrical pacing, and electrical cardioversion. He developed a terminal ventricular arrhythmia and cardiogenic shock and expired on Day 2.

Autopsy Findings: The gastric lumen contained approximately 170 ml of brown fluid admixed with over 40 white tablets. The small and large bowels were remarkable for brown liquid stool admixed with over 60 white tablets. Laboratory analysis of premortun plasma/serum showed venlafaxine 13.5 mg/L and was positive for venlafaxine metabolite and caffeine. The cause of death was determined to be acute venlafaxine intoxication by suicide.

Case 1345. Acute diphenhydramine ingestion: undoubtedly responsible.

Scenario/Substances: 31-y/o male with seizures brought to ED by EMS after suspected diphenhydramine overdose of 2–3 bottles at an unknown time before presentation.

Physical Exam: Male with ongoing generalized seizures.

Laboratory Data: CK 1200 U/L, lactate 33 mmol/L.

Clinical Course: In ED, patient became bradycardic and had a cardiac arrest after arrival and was resuscitated and intubated. He received epinephrine, sodium bicarbonate and amiodarone during the resuscitation with return of spontaneous circulation but hypotensive with continued seizures. He received intralipids (bolus and infusion over 60 min) followed with benzodiazepines and a second intralipid dose (bolus and infusion over 60 min) to terminate seizure activity prior to transfer to the ICU. A third dose of intralipids (bolus and infusion) was administered when hand twitching and hypotension recurred. Ongoing hypotension and poor oxygenation were treated with more intralipids, phenobarbital, phenytoin, benzodiazepines, and then vecuronium ˜12 hrs after admission. Subsequent treatment included levetiracetam prior to development of ARDS with O2 Sat 83% with FiO2 = 1.0. Lab showed troponin 10.7 U/L, phenobarbital 38.4 mcg/mL. The patient's family instituted comfort measures and he expired on Day 3.

Autopsy Findings: Lung: parenchyma congested and red-purple, exuding copious amounts of bloody fluid; Evidence of organ procurement. Postmortem drug concentrations: diphenydramine 3.3 mg/L (peripheral blood). Cause of death: diphenhydramine intoxication. Manner of death: Suicide.

Case 1346. Acute diphenhydramine ingestion: undoubtedly responsible.

Scenario/Substances: A 32-y/o male found seizing at the scene of a low impact motor-vehicle accident; treated by EMS for presumed anaphylactoid reaction with 0.3 mg epinephrine, 10 mg midazolam, and 50 mg of diphenhydramine. Later a suicide note and 2 empty 60 table bottles of diphenhydramine 50 mg were discovered in his vehicle with a receipt dated for that day.

Past Medical History: Schizophrenia and history of “bath salts” abuse; medications included haloperidol and valproic acid.

Physical Exam: Comatose, intubated and unresponsive, pupils 5 mm non-reactive. BP 58/41, HR 58, RR 15, T 40.2°C, O2 sat 98% on 100% FIO2. QRS “markedly prolonged”. PE revealed dry axillae and hypoactive bowel sounds.

Laboratory Data: ABG-pH 6.87/pCO2 63/pO2 252/HCO3 11.5/BE –23, AST 145, ALT 132, INR 0.94, CK 142K;

UDS: cocaine, acetaminophen and salicylates not detected; ethanol 123 mg/dL. Subsequent testing for bath salts and MDPV were negative.

Clinical Course: He received 350 mEq NaHCO3 which was associated with a decrease in the QRS to 106, followed by an NaHCO3 infusion. Tachycardia occurred with a QTc of 541. One dose of activated charcoal was given and levetiracetam was initiated with neurotelemetry. On Day 2, the patient was without seizures and responded to sternal rub while on midazolam 2 mg/h and fentanyl prn. INR 2.15, fibrinogen 129, Cr 2.9, ALT 4,109, AST 10,270, Bilirubin 2.1, CK 35,576 with dark red urine. ECG: QRS 108, QT/QTc 318/451. Day 3: Responded to verbal commands without following commands, anasarca and mottled distal extremities with pupils equal but sluggishly reactive to light; AST 17,339 and ALT 7,052, with worsening acidosis and hyperkalemia. CVVHD was started when CK exceeded 400,000. Empiric antibiotics were given. Day 4: LE bilateral lower extremity fasciotomies were done for possible compartment syndrome. IV NAC was given for AST 7,382, ALT 3,171, T bilirubin 7.3; venous lactate 6.4, CK 178,462. Day 6; MS unchanged, AST and ALT decreasing but bilirubin (total) 11.2. Day 11: no neurologic improvement, irreversible brain injury by MRI; family decided comfort measures only, patient expired within 2 hrs of pressor support discontinuation.

Autopsy Findings: Autopsy not performed. Cause of death was diphenhydramine overdose by the coroner.

Case 1360. Acute-on-chronic, amantadine, diazepam, and clonazepam ingestion: undoubtedly responsible.

Scenario/Substances: A 33-y/o female ingested amantadine 62.5 g, diazepam 15 mg and clonazepam 1.5 mg in an apparent suicide attempt.

Past Medical History: Bipolar disorder and multiple sclerosis.

Physical Exam: BP 137/73, HR 74, asymptomatic female.

Laboratory Data: Ethanol, salicylates, acetaminophen: not detected.

Clinical Course: The patient was transported to the ED at 1.5 hrs post ingestion and was asymptomatic. At 4 hrs post-ingestion, she became acutely disoriented, developed VT, had seizures and cardiac arrest. She was resuscitated with CPR/ACLS, intubation, lidocaine, amiodarone, and physostigmine. Mg and K were also given. On Day 2, she was extubated but remained confused and hallucinating. Reintubation occurred on Day 3 for hypoxia and concern for airway compromise. ARDS ensued with septic shock with positive urine (Escherichia coli), blood (Staphylococcus epidermidis) and sputum (Haemophilus influenza) cultures. She received levofloxacin and continuous infusions of norepinephrine, propofol, midazolam and vecuronium were administered during hospitalization. Pentobarbital was given for refractory seizures confirmed by EEG on Day 14. Comfort measures were instituted on Day 21 when EEG monitoring revealed 252 hrs of persistent seizure activity. The patient subsequently expired.

Autopsy Findings: Not performed. Amantadine serum concentrations: 3,960 ng/mL at 1.5 hrs postingestion, 20,508 ng/mL at 10.5 hrs, 15,508 ng/mL at 21.8 hrs.**

Case 1364. Acute tilmicosin parenteral: probably responsible.

Scenario/Substances: A 51 y/o male injected 5 mL of 300 mg/mL of tilmicosin with suicidal intent. Tilmicosin a macrolide antibiotic for pneumonia treatment in cattle, sheep, and pigs. EMS transported him to the ED.

Physical Exam: Male in full cardiac arrest.

Laboratory Data: Ca 11.4, K 4.4.

Clinical Course: The patient was treated with CaCl2, dopamine and dobutamine with return of spontaneous circulation. He was intubated and placed on a ventilator and demonstrated no response to painful stimuli or blink response. At 9.5 hrs postingestion, BP 135/90, HR109, RR 22. Seizure activity was observed on Day 2, treated with lorazepam and phenytoin. On Day 3, BP 148/79, HR 95, RR 24, T 37.8°C without pressor support. Day 5, he was confused and agitated. BP 168/83, HR 95. A brain MRI showed a recent CVA. His neurologic status did not improve despite cardiovascular stability. Comfort care measures were instituted and he expired on Day 11.

Autopsy Findings: Not Available.

Case 1376. Chronic, theophylline ingestion: probably responsible.

Scenario/Substances: An 82-y/o female presented with weakness, nausea, and trouble breathing, and an elevated theophylline level.

Past Medical History: COPD, diabetes mellitus, and schizoaffective disorder. Medications included insulin, theophylline, paroxetine, fluticasone/salmeterol, albuterol, and meclizine.

Physical Exam: On arrival, she was weak, dyspneic, diaphoretic, and tachycardic, critically ill appearing. O2 sat was 86%.

Laboratory Data: Cr 2.34, initial serum theophylline 83 mg/L, 10 hr 76 mg/L. ECG atrial fibrillation with rapid ventricular response.

Clinical Course: On arrival, she received O2 and IV fluids. Atrial fibrillation with rapid ventricular response persisted so she was treated with multiple IV doses of metoprolol. Once her HR was controlled, she appeared clinically improved, with resolution of nausea and diaphoresis. 10 hr later, her serum theophylline was 76 mg/L and hemodialysis was started. Her clinical status declined markedly, and she was intubated and oxygenated. Her cardiovascular status continued to decline, she suffered a cardiac arrest, resuscitation was unsuccessful, and she expired within 24 hr of admission.

Autopsy Findings: Autopsy was not performed; the hospitalist judged the death was natural, and due to complications of COPD.

Case 1386. Acute flecainide, paroxetine ingestion: undoubtedly responsible.

Scenario/Substances: 29-y/o female ingested 30 tabs of paroxetine and 60 tabs of flecainide in an apparent suicide attempt ˜15 min prior to calling EMS. The patient was found awake and alert with stable vital signs, given oral administered activated charcoal and transported to the ED.

Physical Exam: Alert, awake female, BP 116/78, HR 111 RR 16, O2 sat 98% on room air, fingerstick glucose 96.

Laboratory Data: Full metabolic panel unremarkable.

Clinical Course: Within 30 min of arrival in the ED, the patient developed VT, was intubated during CPR/ACLS and given sodium bicarbonate followed by intralipid bolus and infusion. The patient developed asystole during intralipid administration and received epinephrine, atropine, and sodium bicarbonate and was defibrillated. BP returned but required multiple vasopressors. She was then transferred to a tertiary care center for ICU treatment. Multiple vasorpessors were needed to maintain MAP 30–40, hrs 60: ECG showed wide complex rhythm; the patient was placed on ECMO and given a second bolus and infusion of intralipids at ˜8 hrs after the initial intralipid bolus. No improvement in hemodynamic status was noted. A head CT demonstrated intracranial bleed. The patient expired 29 hrs after initial presentation.

Autopsy Findings: Bilateral necrosis of the globus pallidus, hemorrhagic cavity in left temporal lobe extending into the occipital lobe; full body anasarca. Blood concentrations: premortem, pre-intralipid serum flecainide 1.7 mcg/mL; postmortem: flecainide 36 mg/L (peripheral blood), paroxetine 1.1 mg/L (heart blood). Cause of death: flecainide and paroxetine intoxication. Manner of death: Suicide.

Case 1387. Acute-on-chronic flecainide and ethanol ingestion: undoubtedly responsible.

Scenario/Substances: A 30 yr old male took an intentional overdose of 60 tabs of 100 mg flecaninide.

Past Medical History: Hypertension

Laboratory Data: Ethanol 150 mg/dL, Serum acetaminophen and salicylate not detected.

Clinical Course: He arrived to the ED unresponsive without detectable BP and Pulseless but rhythm was recorded. He had transcutaneous pacer pads placed without capture. An attempt was made to insert a transvenous pacemaker, but he arrested prior to completion of the procedure and resuscitation was not successful.

Autopsy Findings: Postmortem showed sediments in the stomach, pulmonary congestion, cardiomegaly with left ventricular hypertrophy, clinical history of hypertension, and cardiac flecanide level of 24 mg/L. The ME signed the case out as a drug overdose sustained when the patient ingested his flecainide pills. The manner of death was ruled a suicide.

Case 1399. Acute flecainide ingestion: undoubtedly responsible.

Scenario/Substances: 38-y/o woman was in a car, unresponsive in a suspected suicide attempt by overdose.

Past Medical History: Previous suicide attempts by drug overdose, most recently with flecainide a few months prior, treated successfully with intralipids. Medications included: atenolol, clonazepam, oxcarbazepine, paroxetine, folic acid and thiamine.

Physical Exam: Unresponsive female, BP 44/14, agonal breathing, absent gag reflex.

Laboratory Data: ABG-pH 7.28, lactate 7.2,

(*after administration of sodium bicarbonate), acetaminophen 22 mcg/mL (unknown time of ingestion), salicylate not detected; ECG: QRS prolongation.

Clinical Course: Patient was intubated, received IV fluids and benzodiazepines for possible seizure, D50W, sodium bicarbonate, and glucagon 4 mg. Torsade de pointes was treated with Mg (4 g IV) with resolution. Vasopressors were given for hypotension and HCO3 for QRS of 284. Review of prior hospitalization records showed previous suicide attempt with flecainide. At ˜1.5 hrs after ED admission, intralipid bolus and 60-min infusion was given resulting in BP 116/60, HR 120 with continued QRS prolongation. Patient was transferred to the ICU where episodic VT occurred, treated with cardioversion. Hypotension continued, treated with pressors until the patient expired ˜15 hrs. In the ICU, the ECG remained unstable with varying rhythms including short bursts of ventricular tachycardia and was cardioverted successfully. Patient remained hypotensive and vasopressors were switched. ˜15 hrs after ED presentation, the patient expired. Subsequently it was learned that the flecainide was prescribed to the patient's father.

Autopsy Findings: Lungs: congested pulmonary parenchyma with slight to moderate amounts of bloody fluid. Postmortem toxicology from lipemic peripheral blood: flecainide 53 mg/L. Cause of death: flecainide toxicity. Manner of death: suicide.

Case 1550. Acute caffeine energy drink ingestion: contributory.

Scenario/Substances: 14-y/o girl went limp while watching television after drinking from a large container of caffeinated energy drink. She had started with a twitchingand then her eyes were deviated prior to urinary incontinence and loss of consciousness. She was found by EMS to be in VF. After 4 defibrillations, epinephrine and lidocaine she gained return of spontaneous circulation.

Past Medical History: Ehlers-Danlos syndrome, vascular type.

Physical Exam: BP 142/92, HR 129, RR 24, T 37°C.

Laboratory Data: WBC 9; Hgb 14.4; Platelets 355, CK 165,

troponin-I < 0.01, INR 1.0. ECG: sinus tachycardia at 113, T wave inversions in III and aVL.

Clinical Course: She was placed on a ventilator and CT scan head, chest, abdomen and pelvis showed left aspiration pneumonitis without other findings. She received midazolam, propofol, phenobarbital, insulin (for hyperglycemia) and vancomycin. She was transferred to a tertiary care center for pediatric ICU treatment which included therapeutic hypothermia for 24 hrs as well as therapeutic hypernatremia. Repeat CT head showed global diffuse cerebral edema, cytotoxic not vasogenic with obliteration of the cisternal and sulcal spaces throughout. MRI; global anoxic injury. No neurologic recovery was send and the patient expired on Day 7.

Autopsy Findings: CNS: hypoxic-ischemic encephalopathy. Cardiovascular: cardiomegaly, heart weighed 335 g (predicted 206, upper range of normal 311 g); patent foramen ovale; presence of mitral valve prolapse with thickened and redundant leaflets billowing in the left atrial cavity and endocardial thickening of the left ventricle below the posterior leaflet; multifocal contraction band necrosis of the left ventricle with interstitial acute inflammation; coronary arteries normal. Cause of death: Cardiac arrhythmia due to caffeine toxicity complicating mitral valve regurgitation in the setting of Ehlers-Danlos Syndrome. Manner of death: Natural.

Case 1551. Acute magnesium sulfate ingestion: undoubtedly responsible.

Scenario/Substances: A 4-y/o male with multiple chronic health issues was given magnesium sulfate via his gastric tube to loosen his stools after a period of constipation. Several hours later he was seen in the ED with episodes of diarrhea. The child was known to the care team and was discharged from the ED in stable condition. Eighteen hours later he was found prone in his bed cyanotic and unresponsive. EMS found the patient in cardiopulmonary arrest, initiated resuscitation and transport.

Past Medical History: Premature birth at 24 weeks, cerebral palsy, dysphagia with gastric tube placement, chronic constipation.

Physical Exam: Cardiopulmonary arrest, severely dehydrated, NG tubed returned frank blood.

Laboratory Data: BUN 36, Cr 3.3 Na 179, Cl 139, Ca 10.8, K 7.9, Mg 4.5, AST 196 increased to 1759, ALT 155 increased to 1469.

Clinical Course: Resuscitation efforts for greater than 30 min returned a HR and BP, but the patient remained unresponsive. The poison center was contacted after admission to inquire what was in Epsom salts. The patient remained unstable and expired within hr of admission.

Autopsy Findings: Autopsy revealed severe dehydration with electrolyte imbalances, multiorgan failure and disseminated coagulopathy resulting in massive gastrointestinal and adrenal gland hemorrhage. Additional findings included chronic constipation with an acute severe episode of constipation treated with Epsom salts resulting in severe diarrhea, elevated magnesium level, with antemortem blood and postmortem vitreous chemistries consistent with dehydration. The cause of death was declared due to complications of severe dehydration due to severe diarrhea from treatment (Epsom salts) of chronic constipation as a consequence of debilitation/cerebral palsy/premature birth – 24 weeks.

Case 1577. Acute-on-chronic, metformin ingestion: undoubtedly responsible.

Scenario/Substances: A 61-y/o female presented with nausea and vomiting after ingesting 200 metformin tablets (1,000 mg each) 2 hrs prior to EMS arrival. EMS reported that the patient had vomited at the scene and that pill fragments were noted in the emesis.

Past Medical History: Non-insulin-dependent diabetes mellitus, bipolar disorder, and major depression.

Physical Exam: At 3 hrs post-ingestion BP 79/47, HR 74, RR 14 (mechanically-ventilated), T 33.9°C.

Laboratory Data: EMS measured HCO3 was 19; ABG 12 hrs post-ingestion; pH 6.75/pCO2 < 5; BUN 2, Cr 1.1; acetaminophen and salicylate not detected.

Clinical Course: The patient was resuscitated with intravenous crystalloid and developed ventilatory-dependent respiratory failure, metabolic acidosis, and subsequent hypotension in the ED. At 12 hrs post-ingestion she remained unresponsive and required 3 vasopressors for hemodynamic support. Hemodialysis was initiated after the patient received a total of 14 L crystalloid and 6 doses (50 mEq) of sodium bicarbonate. While receiving hemodialysis, the patient was made comfort measures only; she expired ˜17 hrs post-ingestion.

Autopsy Findings: Mild atherosclerosis; lungs with patchy pulmonary edema along with chronic inflammation and emphysematous changes. Postmortem toxicology: metformin 230 mg/L in aortic blood. The medical examiner determined the cause of death to be metformin toxicity.

Case 1580. Acute-on-chronic, insulin parenteral: undoubtedly responsible.

Scenario/Substances: A 71-y/o female was found unresponsive at home. EMS measured glu 15; she received IV dextrose and oxygen and became combative and agitated. GCS improved from 7 to 12 after dextrose. The patient denied being diabetic and was transported to the ED.

Past Medical History: COPD, depression with recent suicidal ideation.

Physical Exam: Unresponsive female, BP 160/98, HR 96, RR 20

Laboratory Data: ABG-pH 7.31/pCO2 40/pO2 172; WBC 13.9,

AST 31, ALT 21, Alk phos 75, Bilirubin 0.3, PT 11, PTT 26.6; CK 116; acetaminophen, ethanol, heavy metals and volatiles not detected; C-peptide 0.6 ng/mL (normal range 0.8–3.5 ng/mL). ECG: sinus tachycardia. Day 2: Blood insulin 83.7 uU/mL (normal range 1.9–23.0 uU/mL).

Clinical Course: The patient was sedated with propofol and intubated. Blood glu was labile, requiring multiple doses of 25 g dextrose IV and a dextrose 20% infusion. Octreotide was administered as sulfonylurea ingestion was initially suspected. Hypotension occurred and sedation was changed to lorazepam without improvement. Blood insulin and C-peptide levels were consistent with exogenous insulin administration. The patient developed aspiration pneumonitis and urinary tract infection, was treated with broad spectrum antibiotics but continued to deteriorate with developing poor cardiac output, oliguria, atrial fibrillation and acidosis despite supportive care. Comfort measures were instituted and she was extubated on Day 41 and expired the following day.

Autopsy Findings: Cause of death; cardiorespiratory complications of insulin-induced hypoglycemia.

Case 1585. Acute-on-chronic, unknown/parenteral: undoubtedly responsible.

Scenario/Substances: A 60-y/o male had received treatment for Hepatitis C with IV alpha lipoic acid infusions at a naturopathic physician's office multiple times previously without problems. During the present treatment, he experienced severe muscle aches, back pain, and fever. He was transported to the ED. Of note, another patient receiving the same infusion at the same office also presented to the ED with similar complaints.

Past Medical History: Hepatitis C, cirrhosis, portal hypertension, diabetes, thrombocytopenia.

Physical Exam: Awake, slightly sedated male patient with severe lower back pain, nausea and vomiting and muscle aches. BP 113/72, HR 125, RR 18, T 39.4°C, O2 sat 97% on room air. pupils equal and reactive, lungs clear, abdomen slightly distended with positive fluid wave; Neuro: motor and sensation intact.

Laboratory Data: Day 1: ABG-pH 7.36/pCO2 38/pO2 105

WBC 6.1, Hgb 8.6, Hct 29, platelets 28, Ca 9.7, Mg 1.9, tot bilirubin 0.8, AST 443, ALT 118, osmol 301, lipase 127, CK 9612, myoglobin 23405, ammonia 279, ferritin 248, transferrin 356, Fe 30. Day 2 ABG-pH < 6.8/pCO2 58/pO2 139; WBC 17.4, Hgb 6.4, Hct 23; Cr 3.5; follow up blood and urine cultures from Day 1 were negative for bacterial growth.

Clinical Course: The patient was admitted to the ICU and remained agitated and restless. Acidosis worsened and was treated with sodium bicarbonate. Hypotension was treated with dopamine unsuccessfully. Soon after intubation the patient became pulseless and was treated with epinephrine, atropine, bicarbonate, and calcium. He regained a pulse but continued to be hypotensive, was treated with multiple pressors and expired on Day 2.

Autopsy Findings: Not available.

Case 1622. Acute-on-chronic, alprazolam and fluoxetine ingestion: undoubtedly responsible.

Scenario/Substances: A 19-y/o female ingested 20–30 alprazolam 1 mg tablets. Her boyfriend reported that she was acting “irrationally” before she took the meds. He found her unresponsive, EMS was called. They found her pulseless and apneic, instituted ACLS resuscitation and intubation. They reported a 10–15 min downtime before a spontaneous HR was regained. She was transported to the ED.

Past Medical History: Bipolar disorder, depression, a previous suicide attempt by cutting her wrists. She was on fluoxetine 40 mg per day and alprazolam 3 mg twice per day. She was known to misuse and abuse the alprazolam.

Physical Exam: Comatose with fixed and dilated pupils, no corneal reflex. HR 91, BP 100/70, T 32.8°C, O2 sat 100% on 100% FIO2 on the hypothermia protocol.

Laboratory Data: K 5.7, Lactic acid 1.0, pH 7.21, pCO2 40, pO2 163, HCO3 15.4, O2 sat 99%, serum acetaminophen, UDS positive for benzodiazepines and THC.

Clinical Course: She was admitted to ICU on a ventilator. Head CT scan showed possible anoxic damage. She was being rewarmed. She was on midazolam, fentanyl, and norepinephrine drips. On neurologic exam, she had no Babinski reflex and no spontaneous respirations, her pupils remained fixed and dilated. On Day 3, a repeat head CT scan showed evidence of diffuse cerebral edema and poor gray white differentiation consistent with early diffuse ischemic changes with an impression of clinical evidence of brain death. A cerebral blood flow study on Day 4 confirmed brain death, preparations were made for her to be an organ donor and she was declared dead.

Autopsy Findings: Cause of death was anoxic encephalopathy from acute alprazolam toxicity. Blood from hospital admission: fluoxetine 49 ng/ml (in deaths attributable to fluoxetine overdose, reported blood or plasma concentrations of parent compound and metabolite range from 2,000 to 11,000 ng/ml.), norfluoxetine 47 ng/ml, alprazolam 130 ng/ml (drug concentrations associated with fatality range from 100 to 400 ng/ml (mean 200 ng/ml.))

Case 1732. Acute 2, 5-dimethoxy-4-ethylphenethylamine, ethanol ingestion and inhalation/nasal: undoubtedly responsible.

Scenario/Substances: A 19-y/o male developed agitation and violent behavior 1 hrs after inhaling 2C-E (4-ethyl-2, 5-dimethoxyphenethylamine) at a party where he had also been drinking ethanol. He subsequently collapsed and became unresponsive. He was driven to the hospital by his friends after they attempted CPR for ˜30 min.

Physical Exam: Cyanotic male; Pulseless, T 40.4°C,

Laboratory Data: Na 150, HCO2 < 4, Cr 2.1, glu 282; Ethanol: 0.06 mg/dL, lactate 32.6, troponin: < 0.01, INR: 2.1; salicylates and acetaminophen: not detected. UDS: positive for ED administered medications, caffeine and cotinine. Urine sample did not have a similar GC-MS ion scan as the purchased stock standard of 2C-E.

Clinical Course: The patient received 1.6 mg naloxone, 4 mg atropine, 5 mg epinephrine, 3 g Ca, and 250 mEq sodium bicarbonate. Intravenous fat emulsion by bolus of 90 mL of 20% solution was administered at 0.75 hrs after ED arrival. Sustained return of spontaneous circulation occurred during the infusion. He received an additional 150 mEq of sodium bicarbonate and infusions of dopamine and norepinephrine. External cooling was initiated but he developed acute respiratory distress syndrome and disseminated intravascular coagulation. He expired several hours after arrival in the ED.

Autopsy Findings: Bilateral hemothoraces, pulmonary edema with bronchopneumonia, cerebral swelling and subendocardial hemorrhage. The Bureau of Criminal Apprehension confirmed the substance as 2C-E. Cause of death: Resuscitated cardiac arrest following witnessed use of 2C-E.

Case 1740. THC homolog ingestion: probably responsible.

Scenario/Substances: A 19-y/o male presented to the ED with confusion, hallucinations, and muscle rigidity. Two containers of bath salts were found in the patient's possesion.

Past Medical History: History of prior bath salt abuse.

Physical Exam: BP 105/27 HR102.

Laboratory Data: BUN 34, Cr 7.8.

Clinical Course: The patient was initialy treated with supportive measures for sympathomimetic toxicity and related complications. Pulmonary embolism was treated with norepinephrine infusion, vasopressin infusion, benzodiazepines, anticoagulation, and hemodialysis. The patient was intubated, ABG-pH 7.4/pCO2 34/pO2 158, O2 sat 99% on ventilator with 35% FiO2. HR was in the 60s, systolic BP 110, and the patient remained unresponsive on the ventilator. On Day 2, the patient again received hemodialysis, Cr 2.4. The patient developed rhabdomyolysis and a repeat brain CT showed worsening cerebral edema. He was resuscitated from the first cardiac arrest, but continued to be unresponsive with fixed and dilated pupils, comfort measures were instituted and he expired.

Autopsy Findings: Postmortem urine was positive for the synthetic cannabinoid metabolite JWH-018 N-(5-hydroxypentyl). No other synthetic cannabinoid metabolites were detected.

Case 1746. Acute-on-chronic benzylpiperazine, lorazepam, marijuana, ingestion, unknown: undoubtedly responsible.

Scenario/Substances: An ICU nephrologist reported a patient thought to have ingested “bath salts” but later possibly thought to have been “transformers.”

Physical Exam: Agitated female

Laboratory Data: ABG-pH 7.29, WBC 2.5, lactate 8.9 mmol/L,

CK 834, myoglobin > 1000, salicylate 2.9 mg/dL, acetaminophen not detected.

Clinical Course: The patient was sedated with propofol, intubated and given sodium bicarbonate infusion for the acidosis. The patient was admitted to the ICU where she remained mechanically ventilated and sedated with no gag reflex and apneic off the ventilator. Follow up labs: ABG-pH 7.32/pCO2 41/pO2 128, Ca 7.3, Mg 2.0,

AST 2638, ALT 3606, WBC 14.2, Hgb 12.1, Hct 35, platelets 108, PT 30.3, INR 2.9, PTT 43.6, fibrinogen 208, d-dimer 18.3 mcg/mL. A hypothermic protocol was initiated; 2 cold caloric tests were administered without positive results, EEG showed no brain activity; the patient expired on Day 3.

Autopsy Findings: The brain was severely swollen and softened; the cerebellar tonsils and medulla were necrotic; microscopic examination of the heart showed focal hemorrhagic infarcts in the papillary muscles; there was bronchopneumonia in the lungs, the liver showed early centrilobular necrosis. Antemortem blood concentrations showed cannabinoids, lorazepam and 5-methoxy-N, N—diisopropyltryptamine (quantified at 27 ng/mL). The cause of death was attributed to severe hyponatremia, and acute and chronic drug intoxication, including 5-methoxy-N,N-Diisopropyltryptamine. The manner of death was concluded to be the accidental ingestion of illicit drugs.

Case 1756. Acute methamphetamine unknown: undoubtedly responsible.

Scenario/Substances: 22-y/o male presented to the ED ˜16 hr after using methamphetamine. He was initially agitated with tachycardia and diaphoresis then became lethargic and hypotensive.

Past Medical History: Methamphetamine use.

Physical Exam: Initially diaphoretic with, HR 200, T 37.7°C.

Laboratory Data: UDS positive for methamphetamine; ECG sinus tachycardia with a QRS of 199, QTc 357. CxR suggested bilateral aspiration versus ARDS.

Clinical Course: Patient was agitated and diaphoretic. He received a total of 10 mg of IV lorazepam and then became lethargic and lost his airway. He was endotracheally intubated and then developed hypotension with a mean arterial pressure of 40. He was given 2 liters of IV fluids and started on norepinephrine. He was placed on a cooling blanket and sedated with additional benzodiazepines. On norepinephrine and dopamine BP 90/47, HR 148, T 38.4°C. Patient remained hypotensive and febrile, then suffered a cardiac arrest and died. A subsequent report from his sister suggested that he had swallowed a plastic bag containing methamphetamine the night before, for unclear reasons.

Autopsy Findings: Intoxication by methamphetamine. Premortem blood methamphetamine 5.63 mg/L, amphetamine 0.16 mg/L, lorazepam 60 ng/mL. Postmortem femoral blood positive for meperidine.

Case 1759. Acute methylone, dextromethorphan, THC homolog, salvia ingestion: undoubtedly responsible.

Scenario/Substances: A 23-y/o, 109 kg male was found in a public area confused and acting erratically. Police were unable to restrain him; the patient was handcuffed prior to transportation to the ED for psychiatric evaluation. Substances labeled Salvia albocaerulea and K2 (herbal blend) were found on the patient.

Physical Exam: In the ED, BP 76/35, HR 145, RR 40, O2 sat 92% (on room air), core T 41.1°C. Combative diaphoretic male with altered mental status requiring restraints. Pupils were unequal and non-reactive; there was blood in his mouth due to a tongue laceration.

Laboratory Data: ABG-pH 7.4/pCO2 22/pO2 207 (non rebreather mask). Ca 9.8, AST 74, ALT 40,

serum osmolality 313; WBC 9.0, Hgb 15, Hct 45, platelets 210; CK 2518, CKMB 17.3, myoglobin > 500 NG/ML, troponin 0.18, PT 11.3, INR 1.1, PTT 21.5; procalcitonin 0.99 ng/ml; acetaminophen and salicylate not detected; UDS negative.

Clinical Course: The patient received IV saline and naloxone (no response) and, due to declining respiratory status, was given vecuronium, intubated and placed on a ventilator. His tongue laceration was sutured prior to having a seizure while in the CT scanner for which he received lorazepam. After central line access was obtained he received norepinephrine, sodium bicarbonate, and electrolyte replacements. A cooling blanket and ice packs were placed. Subsequently he was given levetiracetam, more bicarbonate, phenylepherine, dantrolene, IV hydrocortisone injection and kayexalate. While in the ED, the patient had 4 asystole arrests, was resuscitated and was transferred to the ICU unresponsive. BP 70 s systolic, HR 150 (sinus) with continued IV fluids and pressors. He also received vasopressin, epinephrine, packed RBCs, platelets, vitamin K, one dose of physostigmine, 2 doses of methylene blue and an insulin infusion. Two additional cardiac arrests occurred; he was unable to be resuscitated from the second and he expired on Day 2.

Autopsy Findings: Premortem: dextromethorphan (free and total) 0.02 mg/L; methylone concentrations (hours) were 70 mg/L (0), 0.66 mg/L (3), 0.60 mg/L (8), 0.61 mg/L (13), 0.62 mg/L (25). Postmortem methylone concentrations: 0.84 mg/L peripheral blood, 1.0 mg/L heart blood, 1.4 mg/L ocular blood, 12 mg/L gastric contents, 0.55 mg/L urine. Cause of death: Intoxication by methylone. Manner of death: Accidental.

Case 1762. Unknown, methamphetamine ingestion: undoubtedly responsible.

Scenario/Substances: A 23-y/o male was arrested and spent the night in a holding cell. The next morning he was agitated and received lorazapam 1 mg the evening before admission to the hospital, and 1 mg in the morning at the jain. EMS was called when he became lethargic and found a HR 180. EMS gave lorazepam 1 mg and naloxone 4 mg without response. He was brought to the ED ˜20 hrs after ingestion. He was thought to have ingested 2 methamphetamine “eight balls” the previous day.

Physical Exam: In the ED he was unresponsive with increased muscle tone, BP 83/28, HR 173, RR 40, T 42.0°C (tympanic), diaphoretic, sclerae injected, abdomen: nondistended and nontender.

Laboratory Data: ABG-pH 7.2/pCO2 54/pO2 258, WBC 7.1, Hgb 15.2, platelets 136, EKG: Sinus tachycardia at 171, QRS 112, QTc 502.

calcium 8.2, total bilrubin 0.5, AST 40, ALT 29, Mg 2.1, UDS positive for THC, amphetamines, methamphetamine, and benzodiazepines. Head CT No acute changes.

Clinical Course: The patient was intubated in the ED. He was cooled with ice packs, a cooling blanket, bladder irrigation, and fans, with reduction in T. He was admitted to the ICU where he required vasopressors to maintain BP. He developed DIC with PT > 100. Despite treatment with antibiotics, fresh frozen plasma, and platelets he died Hour 26.

Autopsy Findings: No evidence of trauma. Bilateral hemorrhagic pulmonary edema, acute cerebral edema with bilateral herniation of the cerebellar tonsils and hippocampal gyri. Postmortem blood amphetamine level 0.67 mcg/mL, metamphetamine 22 mcg/mL.

Case 1765. Acute methylone, amphetamines and Synthetic Stimulants, codeine ingestion: undoubtedly responsible.

Scenario/Substances: 24-y/o female ingested “ecstasy” at an electronic music festival. She reportedly had a seizure. EMS found her minimally responsive, HR 132, BP 80/60, administered 5 mg diazepam IV x 2

Past Medical History: Psoriasis

Physical Exam: BP 98/38, HR 159, RR 34, T 41.8°C (oral). Pupils 6 mm equal and minimally reactive, some saliva frothing at the mouth, bilateral rales in all lung fields without wheezes, abdomen unremarkable, flaccid upper extremities and increased tone in the lower extremities with bilateral ankle clonus, withdrew to pain, but was otherwise unresponsive.

Laboratory Data: ABG-pH 7.31/pCO2 35/pO2 280/HCO3 18.1, O2 sat: 100%, lactate 1.9 mMol/L, Troponin I: 0.875.

PTT 23.6, PT 11.1, INR 1.04, urine methylone and butylone confirmed by GC/MS

Clinical Course: In the ED, the patient was nasotrachealy intubated and active cooling measures were begun with ice packs. Hyperactivity and hyperthermia were treated with 2 mg lorazepam and 8 mg midazolam, and she was admitted to the ICU. Head CT was unremarkable. She developed epistaxis and oozing from all IV sites consistent with DIC, and she received packed RBCs and FFP. On Day 2 she she was resuscitated from a PEA arrest, epistaxis and bleeding from her IV sites continued, hypotension required 3 pressors multiple blood products. Based on the prognosis the family opted for institution of comfort measures and he expired on Day 3.

Autopsy Findings: A pill found in her clothing had a powder mass was 619 mg of which 422 mg (68%) was methylone. Butylone was present, but quantation lacked a reference standard. Methylone and ethylone were found in high concentrations in the patient's urine. Autopsy revealed evidence of coagulopathy, fatty liver and anoxic encephalopathy. Cause of death was accidental, secondary to serotonin syndrome.

Case 1772. Amphetamines (synthetic stimulants) inhalation/nasal: undoubtedly responsible.

Scenario/Substances: A 26-y/o male found attempting to enter a stranger's home after using bath salts; he was delirious and eating dirt.

Past Medical History: IV drug abuse.

Physical Exam: Combative, confused patient, shortly after ED arrival had seizures and cardiac arrest. Resuscitated to a tachyarrhythmia (HR 240), was cardioverted successfully but became hypotensive. T (rectal) 41.8°C.

Laboratory Data: UDS: positive for amphetamines, benzodiazepines, opiates and marijuana. At tertiary HCF: pH 7.14, HCO3 11.3, K 3.0, Cr 2.8, CK 64670, CKMB 119, AST 2209, ALT 825, lactate 5.4, troponin I 2.260, WBC 16.2, Hgb 11, Hct 32, platelets 74, urine myoglobin 115 ng/mL, serum myoglobin > 30000 ng/mL; PT 47, PTT 90, INR 8.1, d-dimer > 20 mcg/mL. Day 2 pH 7.08, PCO2 54, K 2.2, Cr 4.6, WBC 14.7, CK 43391, AST 3891 ALT 1889, lactate 5.9, CKMB 163, CK 59070. Day 3 pH 7.0, pCO2 33, Cr 5.2, INR 9.6, platelets 39, lactate 7.6, CKMB 126, CK 43504, AST 10232, ALT 5894.

Clinical Course: After experiencing uncontrollable jerking movements, the patient was transferred to a tertiary HCF where lorazepam, fentanyl and flumazenil were administered. CT head revealed diffuse brain swelling with compression of the ventricular system. He continued to be unresponsive with ARF (acute respiratory failure), severe acidosis, acute kidney injury, DIC, rhabdomyolysis, aspiration and hypokalemia. On Day 3 comfort measures only were instituted and the patient expired that day.

Autopsy Findings: Bilateral hemorrhagic infarction of lung, acute bronchopneumonia with congestion and edema, diffuse hepatic centrilobular necrosis, acute renal tubular necrosis, and diffuse cerebral and cerebellar acute hypoxic changes. Brain findings were consequences of “Excited Delirium Syndrome” associated with MDPV. Blood concentrations: (antemortem) 3,4 methylenedioxypyrovalerone (MDPV) 67 ng/mL; urine concentrations: 3,4 methylenedioxypyrovalerone 4.1 mcg/mL.

Case 1786. Acute THC homolog, caffeine, lidocaine ingestion: undoubtedly responsible.

Scenario/Substances: A 29-y/o, 78.6 kg male started shaking and appeared to faint within 15 min of drinking protein shake powder mixed in creatine water. A friend identified the product as K2 (black incense). EMS on scene witnessed the patient having seizures and administered midazolam 2 mg twice during transport to ED.

Physical Exam: Pulseless, CPR and ACLS in progress in ED. Post resuscitation BP 151/78, HR 133, RR (ventilator) 20, T 37.0°C.

Laboratory Data: ABG-pH 6.76/pCO2 90/pO2 369, O2 sat 98% on 45% FIO2

Ca 10.4, AST 36, ALT 20, WBC 14.5, Hgb 14.6, Hct 46, platelets 416, CK 154, CKMB 2.4 ng/mL, troponin 0.04, ammonia 25, lactate 7.9, PT 16.3, INR 1.32, PTT 27.1, acetaminophen, salicylate, and ethanol not detected on UDS. Lidocaine 2.1 mcg/mL.

Clinical Course: The patient received lorazepam, naloxone, epinephrine, bicarbonate infusion, atropine and was intubated to protect his airway. He remained unresponsive, received intravenous fluids, antibiotics, dexamethasone, nicardipine, esomolol, and TPN. Initial head CT scan was negative; Day 2 repeat CT showed diffuse cerebral edema, without hemorrhage or herniation. Coma persisted for 36 hrs without brainstem reflexes. Family instituted comfort measures only and the patient expired on Day 5.

Autopsy Findings: Anoxic encephalopathy and cerebral edema, pulmonary congestion and edema, myocardial infarction and rhabdomyolysis. Blood Drug Screen from initial blood draw on hospital admission: caffeine 67 mcg/mL, lidocaine 9.6 mcg/mL, monoethylglycinexylidide 3.6 mcg/mL. A specimen of a white crystalline powder in a black plastic bottle labeled as creatine monophosphate detected lidocaine and caffeine by GC/MS, and cocaine and caffeine by LC/MS/MS. Cause of Death: Complications of caffeine and lidocaine ingestion; Manner of Death: Accidental.

Case 1811. Acute methamphetamine inhalation/nasal: undoubtedly responsible.

Scenario/Substances: A 33-y/o male who was known to be smoking “ice” was transported to the ED by the county sheriffs. He was combative but responsive during transit but became unresponsive when reaching the hospital.

Physical Exam: Diaphoretic, agitated male, unresponsive to verbal commands; BP 99/33, HR 150, RR 24, O2 sat 98% on room air.

Laboratory Data: 11.8, AST 50, ALT 42, ethanol 5.0 mg/dL,

UDS positive for amphetamines and THC, salicylate and acetaminophen not detected; CKMB 3.3, myoglobin 1179 ng/ml, troponin 0.08; ECG: sinus tachycardia at 161, QTc 418, QRS 78.

Clinical Course: 30 min after arrival, BP 180/60, HR remaining > 140. The patient received IV saline and lorazepam 2 mg for agitation and tachycardia with minimal response. He was then started on a fentanyl drip. ˜2 hrs later he was intubated. Post-intubation ABG-pH 7.32/pCO2 35/pO2 163. “Posturing” was noted ˜2 hrs later, the fentanyl drip was discontinued and the patient had a fatal asystole cardiac arrest. Axillary temperature at time of death was 36.7°C.

Autopsy Findings: Cause of death: methamphetamine overdose. Postmortem serum methamphetamine 4.1 mg/L.

Case 1820. Acute amphetamines (synthetic stimulant) exposure: undoubtedly responsible.

Scenario/Substances: A 34-y/o male was brought to the ED by EMS for agitated delirium. No exposure history was available, but the agitated delirium was suspected to be from exposure to “bath salts” (synthetic stimulant), because the presentation occurred during an epidemic of exposures with similar presentations.

Laboratory Data: PT > 120, INR > 10, AST 525, ALT 180, CK 16,408, Hgb 14.2, platelets 58, EtOH 24 mg/dL, UDS positive for THC and opiates.

Clinical Course: In the ED HR 180, BP 200/120, T 42.2°C (rectal), disoriented, agitated and dangerously uncooperative. The patient was sedated, endotracheally intubated, ventilated, placed on a cooling blanket, and admitted to the ICU. In the critical care unit, the patient had disseminated intravascular coagulation with oozing from all puncture sites. He received transfusions of blood and plasma. Six hr after admission his T was down to 39.2°C; HR 123, BP 63/25. IV fluid resuscitation was continued but the patient expired in hour 17.

Autopsy Findings: Autopsy: hypertensive cardiovascular disease with cardiomegaly, left ventricular hypertrophy, and nephrosclerosis, pulmonary edema, fatty liver, cerebral edema, and an incidental thyroid nodule. Cause of death was acute intoxication by methylenedioxypyrovalerone (synthetic stimulant. Autopsy also confirmed the presence of lorazepam, morphine and oxycodone.

Case 1831. Acute-on-chronic, amphetamines (synthetic stimulant) exposure: undoubtedly responsible.

Scenario/Substances: A 36-y/o male presented to the ED in cardiac/respiratory arrest following use of an unknown amount of “White Rush Bath Salts” (synthetic stimulant). History was provided by his girlfriend.

Past Medical History: Tourettes, bipolar disease, migraine headaches, and substance abuse. Routine medications included: lithium, venlafaxine, and quetiapine.

Physical Exam: He was apneic, pulseless, pupils were fixed and dilated, his jaw tightly clenched, and abdomen distended. His skin was cool, dry, and deeply cyanotic with moderate dependent lividity, lower extremity joints stiffness suggesting early rigor mortis.

Clinical Course: The patient was given 3 mg epinephrine and 4 mg atropine IV prior to arrival without improvement. He was pronounced dead on arrival to the ED.

Autopsy Findings: The patient's heart had mild to moderate atherosclerosis with chronic inflammation, but was otherwise unremarkable. Urine methylenedioxypyrovalerone > 400 ng/ml, mephedrone not detected. Serum venlafaxine 3105 ng/ml, desmethylvenlafaxine 1121 ng/ml, lithium 0.22 mEq/L, quetiapine 5264 mg/ml, tetrahydrocannabinol 2.2 ng/ml, carboxy-THC 17.9 ng/ml. No other substances were found. The cause of death was ruled MDPV intoxication with atherosclerotic disease. State police visited the store where he purchased the product and obtained a sample of the brand, which was analyzed and found to contain only MDPV.

Case 1841. Acute methamphetamine injection and ingestion: undoubtedly responsible.

Scenario/Substances: A 38-y/o male was found by police in his parked car on a country road with his IV drug paraphernalia. Crystalline material found at the scene tested presumptive positive for methamphetamine. Initially he appeared high, was cooperative and answered questions appropriately, but 3 hr later, after booking, he developed muscle stiffness, diaphoresis, high HR and inablility to answer questions. He was transported to the ED by EMS ˜2 hr later.

Past Medical History: Illicit drug use including IV drug use. He was released on drug charges from jail 2 weeks prior.

Physical Exam: In the ED he admitted to injecting drugs, was diaphoretic, had mydriasis, sinus tachycardia to 190, and BP 151/71 and initially was afebrile. He was treated with IV fluids and lorazepam. While in the ED, he became obtunded, had visual hallucinations, tachypnea (RR 30–40), and hypotension (70/-). He was intubated, a central line was placed, and norepinephrine initially stabilized BP 100–110/-. His T climbed to T 39.6°C treated with a cooling blanket and IV midazolam, but only intermittent neuromuscular paralysis.

Laboratory Data: on admission: Ca 9.1, Mg 2.1,

Amylase 108, AST 53, ALT 112, albumin 4.2, CK 338, CKMB 5.1, troponin1 0.06, UDS positive for amphetamines but negative for other common drugs of abuse; Hour 6 CK 12,744, troponin I 33.1; Hour 13, ABG-pH 7.07/CO2 42/O2 332, FiO2 100%.

Clinical Course: Progressive severe hypotension ensued, despite maximal use of norepinephrine, phenylephrine, albumin and volume administration guided by central venous pressure monitoring. He developed metabolic acidosis, myonecrosis, rhabdomyolysis and oliguria. Echocardiogram showed an EF of 27% and global hypokinesis. He was intubated, ventilated, given sodium bicarbonate. During the night, his HR decreased and he developed asystole. CPR efforts failed and he was pronounced dead Hour 23.

Autopsy Findings: Two plastic bags were found in the stomach and these contained methamphetamine. Antemortem blood sample (untimed) from hospital showed an amphetamine 70 ng/mL, methamphetamine 5775 ng/mL. Postmortem heart blood methamphetamine 34,450 ng/mL, amphetamine 207 ng/mL. GC/MS analysis was positive for caffeine, but was negative for other drugs including benzodiazepines, cocaine, opiates, cannabinoids, carisoprodol, and oxycodone.

Case 1845. Acute amphetamines (synthetic stimulant) exposure: undoubtedly responsible.

Scenario/Substances: A 39-y/o male was brought to the ED after being found outside partially clothed, combative and agitated after admitting to using “bath salts” (synthetic stimulant).

Past Medical History: ethanol abuse, substance abuse, depression and chronic back pain.

Physical Exam: Agitated, extremely combative, diaphoretic, BP 157/74, HR 103.

Laboratory Data: Urine toxicology: positive for PCP and benzodiazepines.

Clinical Course: Patient received diazepam and lorazepam, which briefly decreased his agitation which returned with “psychotic behavior, diaphoresis and ataxia. HR 116. He refused lorazepam IV and received lorazepam and promethazine orally instead. He also was given diphenhydramine by mistake instead of benzodiazepine. He was admitted to telemetry monitoring ˜5 hrs after presentation to the ED. Shortly thereafter he became unresponsive, hyperthermic with HR 200, RR 20 and was transferred to the ICU where T 41.4°C, with jerking movements of the extremities; he was intubated and external cooling measures were started. VT developed and he received amiodarone and diltiazem. HR decreased to 58. At 12 hrs after ED admission he had cardiac arrest and expired.

Autopsy Findings: Neuropathology was unremarkable; Lungs: parenchyma congested with red-purple exuding moderate amounts of bloody fluid; Liver: capsule was smooth, moderately congested parenchyma with no focal lesions. Postmortem toxicological analysis: methylenedioxypyrovalerone (MDPV) 1.0 mg/L in peripheral blood; mephedrone and phenycyclidine not detected; methcathinone not assayed. Cause of death: MDPV intoxication. The manner of death: accidental.

Case 1851. Acute amphetamine (synthetic stimulant), trimethoprim, and ethanol inhalation/nasal, parenteral: undoubtedly responsible.

Scenario/Substances: A 40-y/o male was found agitated, naked, and delusional and running around after using a “bath salts” (synthetic stimulant). He required 2 applications of an electroshock device to control before being brought to the hospital.

Past Medical History: Bipolar disorder and drug abuse. Medications reported as quetiapine, methadone, temazepam and 10/650 mg hydrocodone/acetaminophen.

Physical Exam: Agitated, yelling incomprehensibly, male patient; BP 131/72, HR 164, RR 24, T (oral) 36.7°C, O2 sat 100% on a non-rebreather; Pupils dilated.

Laboratory Data:

UDS: positive for opiate, negative for cocaine, phencyclidine, amphetamine, tetrahydrocannabinol, benzodiazepines and barbiturates; salicylates 4.1 mg/dL, acetaminophen and ethanol not detected; INR 1.0, CK 234, AST 19, ALT 36. 5 hrs later: Venous blood gas; pH 7.2/pCO2 39/pO2 35; HCO3 16.2, AST 869, ALT 738, PT 47.2, INR 4.2, CK 14,839, Hgb 11.5, platelets 56, troponin I 5.22, lactate25.5. 10 hrs after presentation: ABG-pH 7.14/pCO2 30/pO2 119; HCO3 10; LDH 11,108, TSH 2.21 mIU/L with a free thyroxin of 1.10 ng/dL, factor VIII assay 31%, ammonia 150 umol/L. At 24–28 hrs: Hgb 7.1, platelets 11, AST 10873, ALT 6629, CK 75,952, INR > 9.3.

Clinical Course: Shortly after arrival in the ED, the patient was placed on a cardiac monitor and developed bradycardia and subsequent cardiac arrest. He received 2 doses of 1 mg epinephrine and 1 mg atropine, as well as 100 mg lidocaine, 2 mg of naloxone and 0.5 mg of flumazenil IV. After 30 min, he had return of spontaneous circulation; dopamine and phenylephrine infusions were started for hypotension. T (rectal) 40.8; GCS 3; his pupils were dilated. He was given IV fluids (7 L NS) and transferred to a tertiary care center. At the second HCF he remained hypotensive; norepinephrine was initiated, T 37.9°C, HR 114, RR 32 (ventilator rate set at 20), O2 sat was100%. He responded to painful stimuli; pupils were minimally reactive to light, gag reflex was present. Needle marks were noted on the patient's arms and the patient was oozing from his IV sites. ECG: HR 53 with peaked T waves, QRS 158 and QTc 420. He was treated for hyperkalemia (K 8.0) with 1 g Ca gluconate, 10 U insulin, 50 g dextrose and 50 mEq sodium bicarbonate. He developed worsening metabolic acidosis and rhabdomyolysis with oliguria then anuria; antibiotics were initiated for a right upper lobe consolidation. Subsequently he developed DIC and melanotic stools. Phytonadione, and multiple blood products were given and he received hemodialysis. Head CT showed cerebral edema and anoxic injury; EEG: anoxic injury and ultimately the patient was declared brain dead. Comfort measures were initiated and he expired ˜42 hrs after presentation.

Autopsy Findings: Not performed. Antemortem blood from first HCF: MDPV 0.31 mg/L, other samples from the second HCF: MDPV urine: 670 ng/mL; serum 82 ng/mL. Trimethoprim: urine 12 mcg/mL; serum 2.2 mcg/mL. Clonazepam 0.006 mg/L,7-aminoclonazepam not detected; methadone, hydrocodone, cocaine, ethanol, and gabapentin not detected. Cause of death: excited delirium secondary to MDPV ingestion.

Case 1917. Acute methamphetamine and phencyclidine ingestion: undoubtedly responsible.

Scenario/Substances: A 51-y/o male was arrested for drug possession. While in custody, he became agitated and belligerent. He also had an episode of bowel incontinence, during which he passed a 2-gram baggie of methamphetamine. EMS was called for transport to an ED. While in the ambulance bay at the hospital, the patient was undressing and speaking “gibberish” when he suddenly became unresponsive, pulseless, and was found to be in PEA arrest.

Past Medical History: Chronic hepatitis C.

Physical Exam: The patient was covered in feces, GCS 3, pupils 5 mm fixed and dilated, T 40.2°C (rectal).

Laboratory Data: HCO3 20, anion gap of 19, lactate 13.1 mmol/L, AST 61, ALT 123, PT 15.7, INR 1.3. Initial ABG-pH 7.03/pCO2 63/pO2 333/HCO3 16.5/BE 14.4.

Serum acetaminophen and salicylates were not detected. UDS positive for amphetamine and methamphetamine, cocaine and/or metabolites, and phencyclidine (all confirmed by GC-MS).

Clinical Course: Intubation, CPR and epinephrine 1 mg IV × 2 restored a HR 30–40 after about 5 min. He then had another episode of PEA arrest. After atropine 1 mg IV × 3 and epinephrine 1 mg IV spontaneous circulation returned, although with persistent hypotension, for which he was started on dopamine and norepinephrine. He was admitted to the ICU, where he remained comatose without any pupillary, corneal, cough or gag reflex. A head CT showed significant diffuse cerebral edema with loss of gray-white junction and herniation into foramen magnum. No significant abnormalities were identified on abdominal/pelvic CT scan. On Day 2 he was determined to be brain dead, based on an apnea test, the brainstem reflex exam, and isoelectric EEG. BP could not be maintained despite maximum pressor doses, he expired.

Autopsy Findings: 1) Marked cerebral edema with uncal herniation; 2) marked pulmonary edema; 3) evidence of systemic hypertension: mild cardiomegaly, concentric left ventricular hypertrophy, slight arterionephrosclerosis; 4) chronic viral hepatitis (anamnestic). Postmortem toxicology report from peripheral blood were positive for methamphetamine 21,000 ng/ml, amphetamine 700 ng/ml and phencyclidine 64 ng/ml. The cause of death was acute methamphetamine, amphetamine, and phencyclidine intoxication.

Abbreviations & Normal ranges for Abstracts

Disclaimer – all laboratories are different and provide their own normal ranges. Units and normal ranges are provided here for general guidance only. These values were taken from Harrison's,10 Goldfrank11 or Dart.12

serum electrolytes have units of mEq/L = mmol/L

˜ = approximately

ABG-pH/pCO2/pO2/HCO3/BE

ABG = arterial blood gases

ABG-pCO2 = partial pressure of carbon dioxide [38–42]

ABG-pH = hydrogen ion concentration [7.38–7.42]

ABG-pO2 = partial pressure of oxygen [90–100]

ACLS = advanced cardiac life support, protocol for the provision of cardiac resuscitation

AICD = automatic implanted cardiodefibrillator

Alk phos = alkaline phosphatase [13–100] U/L

ALT = Alanine aminotransferase [7–41] U/L = (SGPT)

AMA = against medical advice

Ammonia = [25–80] mcg/dL = [15–47] mcmol/L

amp = ampoule

APLS = advanced pediatric life support, protocol for the provision of cardiac resuscitation

ARDS = acute respiratory distress syndrome

AST = Aspartate aminotransferase [12–38] U/L = (SGOT)

AVblock = atrio-ventricular block

BAL – British anti-Lewisite

BE = base excess, mmol/L

Bicarbonate = [22–26] mEq/L

Bilirubin = total [0.3–1.3] mg/dL, direct [0.1, 0.4] mg/dL, indirect [0.2, 0.9] mg/dL

BLQ = below the limit of quantitation

BMI = body mass index

BP = Blood Pressure, systolic/diastolic, (Torr)

BUN = see Urea nitrogen

C = degrees Centigrade

Ca = calcium, [8.7–10.2] mg/dL

CABG = coronary artery bypass graft

CAD = coronary artery disease

CIWA = Clinical Institute Withdrawal Assessment for Alcohol

CK = creatinine kinase (CPK), total: [39–238] U/L females, [51–294] U/L males

CKMB = MB fraction of CK [0.0–5.5 mcg/L = 0.0–5.5 ng/mL]

Fraction of total CK activity [0–0.04 = 0–4.0%]

Cl = chloride [102–109] mEq/L

CNS = central nervous system

COHb = carboxyhemoglobin

COPD = chronic obstructive pulmonary disease

CPR = cardio pulmonary resuscitation

Cr = creatinine [0.5–0.9] mg/dL females, [0.6–1.2] males

CRRT = continuous renal replacement therapy

CSF = cerebrospinal fluid

CT = computed tomography (CAT scan)

CVA = cerebrovascular accident

CVVHD = continuous venovenous hemodiafiltration

CxR = chest radiograph, chest xray

D10W = 10% dextrose in water

D50W = 50% dextrose in water

D5NS = 5% dextrose in normal saline

D5W = 5% dextrose in water

Day = when capitalized, Day = hospital day, i.e., days since admission

DIC = disseminated Intravascualar coagulation

Dx = diagnosis

ECG = electrocardiogram (EKG), leads = I, II, III, aVR, aVL, aVF, V1, V2, V3, V4, V5, V6

ECMO = extracorporeal membrane oxygenation

ED = emergency department, in these abstracts refers to the initial health care facility

EDDP = principal methadone metabolite, 2-ethylidene-1,5-dimethyl-3, 3-diphenylpyrrolidine

EEG = electroencephalogram

EF = ejection fraction

ELISA = enzyme-linked immunosorbent assay

EMS = emergency medical services, paramedics, the first responders

ER = extended release (sustained release)

FFP = fresh frozen plasma

FiO2 = fraction of inspired oxygen

g = grams

g/dL = grams per deciliter

GCS = Glasgow Coma Score, ranges from 3 to 15

GERD = gastroesophageal reflux disease

GI = gastrointestinal

Glu = glucose, fasting [75–110] mg/dL

HCF = health care facility

HCG = human chorionic gonadotropin test for pregnancy

HCO3 = bicarbonate

HCP = health care provider

Hct = hematocrit [35.4–44.4] females, [38.8–46.4]% males

Hgb = hemoglobin [12.0–15.8] g/dL females, [13.3–16.2] g/dL males

HIV = human immunodefficiency virus

Hour = when capitalized, Hour = hours since admission

HR = HR, beats per min

hrs = hours

ICU = intensive care unit

IgE = immunoglobulin E

IM = intramuscular

INR = international normalized ratio (PT to control) [0.8–1-2]

IU/L = international units per Liter

IV = intravenous

K = potassium, [3.5–5] mEq/L

kg = kilogram

L = Liter

Lactate = lactic acid [4.5–14.4] mg/dL arterial, [4.5–19.8] mg/dL venous

LBBB = left bundle branch block on ECG

Leukocyte = white blood count [3.54–9.06] 103/mm3 count

m/o = months old

MAP = mean arterial pressure

mcg/dL = micrograms per deciliter

mcg/L = micrograms per Liter

mcg/min = micrograms per minute

mcg/mL = micrograms per milliliter

mcmol/L = micromoles per liter

MDA = 3,4-methylenedioxyamphetamine

MDMA = methylenedioxymethamphetamine (ecstasy)

ME = medical examiner

mEq = milliequivalents

mEq/L = milliequivalents per Liter

Mg = magnesium [1.5–2.3] mg/dL

mg = milligrams

mg/dL = milligrams per deciliter

mg/kg = milligrams per kilogram

mg/L = milligrams per Liter

min = minutes

mmol/L = millmoles per Liter

mosm/kg = milliosmoles per kilogram

mosm/L = milliosmoles per Liter

MRI = Magnetic Resonance Imaging

ms = milliseconds

Narrative Headers:

Scenario/Substances: concise narrative of EMS & pre-HCF events

Past Medical History: available relevant past medical history

Physical Exam: initial physical exam if available

Laboratory Data: initial results, give units except for units given in abbreviations

Clinical Course: concise narrative of HCF & beyond with outcome

Autopsy Findings: = medical examiner and/or autopsy results

NG = nasogastric

ng/mL = nanograms per milliliter

not detected = analyte below the level of quantitation, negative

NPO = nil per os, nothing by mouth

NS = normal saline

O2 sat = oxygen percent saturation [94–100]% at sea level

OR = operating room

Osm = osmole

PALS = pediatric advanced life support

PC = poison center ( = PCC, or Poison Control Center)

PCC = prothrombin complex concentrate

PCP = primary care provider

PEA = pulseless electrical activity

PEEP = positive end expiratory pressure

PICU = pediatric intensive care unit

Platelets = platelet count [150–400] ×109/L

PO = per os (“by mouth” in Latin)

Potassium = [3.5–5] mEq/L

Ppm = parts per million

PR = P-R interval [120–200] msec on the ECG

prn = as needed

PT = prothrombin time, INR is preferred, but PT may be used if INR is not available

PTA = Prior to admission

PTT = partial thromboplastin time [26.3–39.4] sec

QRS = ECG QRS complex duration [60–100] msec

QT = Q to T interval on the ECG waveform, varies with HR

QTc = QT interval corrected for HR, usually QTcB = QT/RR½ (Bazett correction) 1–15 y-o [< 440] msec, adult male [< 430] msec, adult female [< 450] msec

RBBB = right bundle branch block on ECG

RBC = red blood cell(s)

RR = respiratory rate, breaths per minute

s/p = status post

sec = seconds

SL = sublingual

SVT = supraventricular tachycardia

Synthetic = one or more of the products (6-APB, Stimulant bath salts, plant food, Bliss, Ivory Wave, Purple Wave, Vanilla Sky, et al) or chemicals (3,4 methylenedioxypyrovalerone [MDPV], 6-(2-aminopropyl)benzofuran [6-APB], butylone, desoxypipradrol [2-DPMP], ethylone, flephedrone, naphyrone, mephedrone, methylenedioxypyrovalerone, methylone, methcathinone, et al)

T (oral) = Temperature (oral) [36.4, 37.2]°C or

T (rectal) = Temperature (rectal) [36.4, 37.2]°C or

T (tympanic) = Temperature (tympanic) [36.4, 37.2]°C

THC = tetrahydrocannabinol

THC Homolog = one or more of the products (Blaze, Dawn, herbal incense, K2, Red X, spice, et al) or chemicals (cannabicyclohexanol, CP-47,497, JWH-018, JWH-073, JWH-200, et al)

TPN = total parenteral nutrition

Tprot = total protein

Troponin I = normal range [0–0.08] ng/mL, Cut-off for MI > 0.04 ng/mL

U/dL = units per deciliter

U/L = units per liter

U/mL = units per milliliter

UA = urinalysis

UDS = urine drug screen

Urea nitrogen = [6–17] mg/dL (BUN)

VBG = venous blood gasses

VF = Ventricular fibrillation

VT = Ventricular tachycardia

WBC = white blood count, see leukocyte count

WNL = within normal limits

y/o = years old

Supplemental material

http://informahealthcare.com/ctx/10.3109/15563650.2012.746424

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References

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