Barry J. Knapp, MD

Approximately 6.5 million adults in the United States have heart failure, accounting for nearly 1 million ED visits annually.¹Advanced heart failure is particularly difficult to treat, and is associated with significant morbidity and mortality. While medical therapy is the initial treatment for patients with advanced heart failure, it has limited effectiveness; therefore, at the present time, heart transplant is the most effective treatment for heart failure refractory to medical management.

According to the 2013 Registry of the International Society for Heart and Lung Transplantation, 4,096 cardiac transplants were performed worldwide in 2011, approximately 2,000 of which were done in the United States.²

The average age of a heart transplant recipient in the United States is 55 years.² In 2017, there were nearly 4,000 patients on the United Network for Organ Sharing, the organization that manages the national transplant waiting list in the United States and matches donors to recipients.³ Unfortunately, the number of patients requiring a heart transplant far exceeds the number of registered donors, and a large number of patients must wait years for transplantation. In addition to those awaiting a heart transplant, there are many patients with advanced heart failure who are not suitable candidates for transplant (usually due to age).

Left Ventricular Assist Devices

As of December 31, 2016, a total of 22,866 US Food and Drug Administration (FDA)-approved devices were listed in the Interagency Registry for Mechanically Assisted Circulatory Support, 17,016 of which were continuous-flow (CF) left ventricular assist devices (LVADs), including the HeartMate II (HMII) (Abbott Laboratories) and the HeartWare Ventricular Assist Device (HVAD) (Medtronic).⁴ Left ventricular assist devices, which have been in use for over 30 years, have evolved into smaller, quieter, and more durable devices. The current generation of LVADs has a CF design (as opposed to the older pulsatile-flow [PF] design). More importantly, CF LVADs are associated with higher survival rates and increased quality of life than the earlier PF models.⁵For these reasons, CF LVADs are being used much more frequently today. As previously noted, LVADs serve as a temporizing measure for patients awaiting a heart transplant (ie, bridge-to-transplant therapy [BTT]) or as the primary treatment for patients who are not suitable candidates for transplant (ie, destination therapy [DT]).

The percentage of patients receiving an LVAD as a DT has increased from around 15% between 2006 to 2007 to nearly 46% in 2014.⁶Recently, several reports following LVAD patients demonstrated a reverse remodeling of the heart and recovery of native cardiac function that was sufficient enough in some patients as to permit LVAD removal (ie, bridge to recovery).⁷ In the United States, the number of patients undergoing LVAD removal due to recovery remains fewer than 3%.⁶With the increase in the number of patients receiving LVADs, there is an increased likelihood of LVAD patients presenting to an ED due to device-related complications. Recognized complications associated with LVADs include thrombosis, infection, bleeding, and issues with volume status.^5,7 However, the frequency of LVAD-associated complications and the final disposition of these patients is less well known.

HeartMate II Patient ED Presentation Study

Purpose

The purpose of our study was to identify the reasons for LVAD patient presentation to the ED, the frequency of these presentations, and the final disposition of these patients. Our institution, Sentara Norfolk General Hospital (SNGH), is a level I trauma and a tertiary care referral center, and it is the only hospital in a large area of Virginia to perform LVAD implantation.

Our study involved only patients implanted with the HMII LVAD.

Methods

Patients and Study Design

This was a retrospective study of patients with an HMII LVAD who presented to the SNGH ED between April 1, 2009 and September 9, 2012. All patients implanted with an HMII LVAD during the study period were assigned a study number linking the patient to their medical record number and social security number. Study numbers were assigned at the time of LVAD implantation by one of the investigators. This document was kept in a secure and locked location in the department of emergency medicine and was not accessible to anyone other than study investigators.

The electronic medical records were retrospectively reviewed to identify any HMII LVAD patient presenting to the SNGH ED during the study period. Information abstracted from the ED medical records included patient age, sex, initial complaint, final diagnosis, and disposition. Only the patient’s assigned study number was used on the data collection form, and no personal identifying information was present.

This study was granted approval for human subject research by the Eastern Virginia Medical School Institutional Review Board. Eligible patients included all patients with an HMII LVAD implanted during the study period. Study patients who presented to the SNGH ED between April 1, 2009 and September 9, 2012 were identified by a retrospective chart review. These patients were instructed to specifically seek care at the SNGH ED in the event of an emergency. There were no exclusion criteria.

Data were collected and reported in real numbers and percentages. No formal statistical analysis was used in evaluating the results.

Results

Between April 1, 2009 and September 9, 2012, there were a total of 98 patients with an HMII LVAD that had been implanted during the study period at SNGH. The average patient age was 53.6 years, with a range from age 20 years to 78 years. Sixty-seven (68%) of the patients enrolled in the study required at least one ED visit. The HMII LVAD patients who presented to the ED ranged in age from 20 years to 78 years, with an average age of 53.1 years. The average number of ED visits by these 67 patients was 3.7, with a range of 1 to 12. Approximately 56% of the ED visits were directly LVAD-related. In all, 67 patients were responsible for a total of 248 ED visits.

The two most common reasons for presentation to the ED involved bleeding and volume overload. A total of 37 ED visits (14.9%), were related to bleeding, which included gastrointestinal (GI) bleeding (18/37 or 49%), epistaxis, hematuria, gingival bleeding, and postoperative bleeding following tooth extraction.

Volume overload accounted for 37 ED visits (14.9%), and the most common presenting symptom in these patients was shortness of breath. Other reasons patients presented to the ED were weakness/lightheadedness/dizziness/syncope (24/9.6%), device malfunction (20/8.1%), infection (7/2.8%), and transient ischemic attack/cerebrovascular accident (6/2.4%). For infection-related ED visits, two presentations (2.9%) involved a driveline infection. Common causes for ED visits related to device malfunction included battery failure and device-alarm activation. Overall, 142 of the 248 total ED visits (57.3%) resulted in hospital admission. One patient in the study presented in cardiac arrest and could not be resuscitated.

The remaining 108 LVAD patient ED visits (44%), did not appear to be related to the presence of the LVAD, but rather represented common reasons for presentation to an ED. These other non-LVAD-related reasons for presentation to the ED were due to motor vehicle incidents (3); assault (2); dental pain (3); mechanical fall (5); and upper respiratory tract infection (4), and represented small groupings of patient reasons for an ED visit.

Examples of singular reasons for presentation to the ED included one patient who presented with suicidal ideation, and another patient who presented for evaluation of symptoms suspicious for a sexually transmitted infection.

Discussion

As the number of patients with advanced heart failure continues to increase, the number of those with an LVAD also increases. Between 2006 and June 2013, nearly 9,000 adult patients in the United States received a durable LVAD.⁶ In the early years of LVAD implantation, patients were restricted to remain in proximity of geographical areas surrounding academic health care centers. An increased comfort level by both physicians and patients now allows LVAD patients to reside in more distant communities. This increase in LVAD implantation, coupled with the widening patient distribution, make it important for every emergency physician (EP) to have a working knowledge of the device and its associated complications. To date, the characteristics and frequency of LVAD patient presentations to the ED have not been well characterized.

Left ventricular assist devices are considered in patients who have significant symptoms associated with poor LV function or who cannot maintain normal hemodynamics and vital organ function. Continuous-flow LVADs account for almost all devices currently implanted. During our data-collection period, there were two FDA-approved implantable LVADs—the HMII, approved for BTT in 2008 and for DT in 2010; and the HVAD approved for BTT in 2012. In August 2017, HeartMate III (Abbott Laboratories) was approved by the FDA. All patients enrolled in our study were recipients of the HMII device, as this was the only type of LVAD implant performed at our hospital. Current survival with the HMII LVAD is 80% at 1 year and 69% at 2 years, and there has not been shown to be a significant difference when stratified by era of implant.⁶

Device Designs and Structures

The pump of the HMII is inserted into the abdominal cavity, whereas the HVAD is implanted in the chest cavity, with the inflow cannula in the apex of the LV and the outflow cannula connecting to the proximal aorta. Blood is continuously pumped through the system.^8,9 The pump is connected to a driveline that exits the body and connects to a controller. Continuous-flow devices have either an axial or centrifugal blood pump. Axial devices have an impeller that is connected to ball-and-cup bearings that accelerate blood along its axis. Newer axial flow pumps incorporate magnetic levitation of the rotor and do not require the use of bearings. Centrifugal devices accelerate blood circumferentially with a rotor that is suspended within in the blood pool by electromagnetic or hydrodynamic forces.¹⁰ The controller is powered by two external batteries or connected to a power base unit where the pump can be interrogated. The controller is usually housed in a garment worn by the patient, one that also includes the batteries. The controller can also be powered by a base unit that can be plugged into an electrical outlet.¹¹

There are, and continue to be, advances in both LVAD design and function. Since the time period of our study, changes have been made in the outflow bend relief (the tube at the junction of the outflow cannula and the pump housing designed to prevent kinking of the outflow cannula) and the LVAD controller. Older controllers have been replaced with newer models, but many of the LVAD pumps in this article remain in service.

Anticoagulation Therapy

Patients who have a CF LVAD require anticoagulation therapy with warfarin to a target international normalized ratio (INR) of 2 to 3, in addition to aspirin therapy of 325 mg daily.^8,9Newer oral anticoagulant drugs are not routinely given to patients who have a CF LVAD.

Cardiopulmonary Evaluation

With CF LVADs, blood is pumped continuously, and a constant, machine-like murmur can be heard on auscultation rather than the typical heart sounds. Patients who have an LVAD may not have palpable arterial pulses. Doppler evaluation of the brachial artery and a manual blood pressure (BP) cuff are used to listen for the start of Korotkoff sounds as the cuff is released. The pressure at which the first sound is heard is used to estimate the patient’s mean arterial pressure (MAP) at the time when there is no pulse; and the systolic BP (SBP) is heard at the time when there is pulse. Patients with a CF LVAD with nonpulsatile flow should have a MAP between 70 mm Hg and 90 mm Hg (HMII), or 70 mm Hg and 80 mm Hg (HVAD). Patients who have a CF LVAD with a palpable pulse should have an SBP less than 120 mm Hg (HMII) or 105 mm Hg (HVAD). Readings outside of these ranges require an adjustment in the patient’s antihypertensive therapy, since high BP increases the risk of stroke and can impair the cardiac support provided by the LVAD.⁸Low BP may be the result of inadequate pump speed, dehydration, inflow cannula obstruction, or pump thrombus.

Bleeding

In our study, bleeding and volume overload were the two most common reasons LVAD patients presented to the ED. Interestingly, in a systematic review of clinical outcomes following CF LVAD implantation, bleeding was the most commonly recorded adverse event.¹²In fact, the majority of patients in all of the studies reviewed experienced at least one bleeding event. In one study of 139 HMII LVAD patients, the risk of bleeding was greatest within the first two weeks, and early bleeding was associated with increased mortality.¹³The most common source of bleeding complications in patients with a CF LVAD are GI, similar to our study.¹⁴

In a review and meta-analysis by Draper et al,¹⁵of GI bleeding in 1,697 patients with CF LVADs, the pooled prevalence was 23%.Subgroup analysis demonstrated an increased risk of bleeding in older patients and in those who had an elevated serum creatinine level.¹⁵Upper GI bleeding occurred in 48% of patients, lower GI bleeding in 22%, small-bowel bleeding in 15%, and bleeding at an unknown site in 19%. The most common cause of the bleeding was from arteriovenous malformations (AVMs).¹⁵In their review, Draper et al¹⁵ found a 9.3% prevalence of recurrent GI bleeding and a pooled event rate for an all-cause mortality rate of 23%.

They also noted that the increased risk of GI bleeding in CF LVAD patients is multifactorial. For example, there was decreased activity of type 2 von Willebrand factor multimers in patients with CF LVADs, leading to an acquired von Willebrand syndrome.¹⁵

Another finding seen in this review was that CF devices lead to a low pulse-pressure system, which is thought to cause some degree of intestinal hypoperfusion, potentially leading to vascular dilation and AVM formation.¹⁵Based on findings, a neurovascular etiology involving increased sympathetic tone resulting in smooth muscle relaxation and AVM formation has been proposed. Lastly, the anticoagulation required with the CF LVADs to prevent pump thrombosis also increases the risk of GI bleeding, especially when combined with aspirin or other antiplatelet agents which are routinely prescribed.¹⁵

Volume Overload

Interestingly, in our study, volume overload as a cause for ED presentation was the same as for bleeding complications. In the systematic review of clinical outcomes in CF LVAD patients, volume overload or ongoing heart failure occurred in 18% of patients 1 year after device implantation.¹²

The clinical presentation of patients experiencing volume overload is typically dyspnea and fatigue; on physical examination they will frequently demonstrate evidence of fluid retention, such as dependent edema and pulmonary congestion.¹⁶Causes of volume overload in the LVAD patient includes medication noncompliance, inadequate pump speed, device malfunction, right ventricular failure, impaired renal function, and cardiac tamponade.¹⁶ These patients will frequently have MAPs greater than 90 mm Hg, and may require treatment with diuretics, calcium channel blockers, beta-blockers, or angiotensin-converting enzyme inhibitors.⁸

Weakness, Lightheadedness, Dizziness, Syncope

In our study, some combination of weakness, lightheadedness, dizziness, and syncope accounted for the third most common cause of ED presentation (9.6%). In the majority of cases, this was due to dehydration. Usually, these patients will have a MAP less than 60 mm Hg. Unfortunately, patients with pump thrombosis, sepsis, or cannula malposition can also present with a low MAP. It is important to differentiate the cause, as the management is quite different, depending on the etiology. Bedside ultrasound can play an important role in evaluating the volume status and cannula position.⁸ In addition, emergent consult with the patients ventricular assist device (VAD) treatment team is critical.⁸ Pump thrombus is a medical emergency and is usually associated with hematuria without red blood cells in the urine, acute kidney injury, and marked elevations in lactate dehydrogenase and serum free hemoglobin.⁸ If not treated promptly, renal failure and death may result. If dehydration is the cause, gentle rehydration with intravenous normal saline and electrolyte replacement may be all that is required.

Device Malfunction

Device malfunction was the next most common reason for ED presentation in our study, at 8.1%. This category included a number of different events, including battery failure, driveline fracture, and pump thrombosis. According to McIlvennan et al,¹² causes of device malfunction include thrombus formation with hemolysis, mechanical failure of the impeller, and driveline lead fractures with electrical failure.Again, the VAD team should be consulted immediately, and the EP should plug the LVAD into a hospital power base, if available, to conserve battery life. If power is interrupted, the pump will stop working. The EP should examine all of the connections from the percutaneous lead to the controller and from the controller to the batteries to ensure they are intact. The exit site for the percutaneous lead should be examined for evidence of trauma or signs of infection. The patient should also be asked about recent trauma to the driveline.

Neurological Events

Interestingly, in other reviews, neurological events, including ischemic stroke, hemorrhagic stroke, and transient ischemic attack occur with higher frequency than was the case in the study, and are relatively common complications that can result in severe morbidity and mortality.¹²In the Interagency Registry for Mechanically Assisted Circulatory Support report, there was a 3% risk of stroke at 1 month, 5% at 3 months, 7% at 6 months, 11% at 12 months, 17% at 24 months, and 19% at 36 months post-implant.^6,12Similarly, the HMII DT Trial demonstrated rates of ischemic and hemorrhagic stroke as high as 8% and 11% respectively, within the first 2 years following LVAD placement.^5,6In our study, neurological events accounted for only six (2.4%) of ED visits. It is unclear why our numbers were less than those reported by others.

Cardiac Events and Management

During the study period, one LVAD patient presented to the ED in cardiac arrest. Patients who have an LVAD and are in cardiac arrest have unique considerations that deserve discussion. If the LVAD pump has stopped functioning, connections between the system controller and the pump and power source must be checked, as loose connections need to be refitted and the pump restarted. It is important to note that when an LVAD ceases operation, blood becomes stagnant in the pump and conduits. Delays of even several minutes pose a significant risk for pump thrombosis, stroke, and thromboembolism when the device is restarted. If the pump does not restart and the patient is connected to batteries, the batteries should be replaced with a new, fully charged pair, or the device should be connected to a base unit.¹⁷

Due to the location of the outflow graft on the aorta and the inflow conduit in the LV apex, external chest compressions pose a risk of dislodging the device and causing fatal hemorrhage. Clinical judgment should be used when deciding to perform external chest compressions. A recent American Heart Association scientific statement concluded that withholding chest compression in a patient with an LVAD who is truly in circulatory failure that is not attributable to a device failure would cause more harm to the patient than the potential to dislodge the device.¹⁸

Direct cardiac massage, performed by a skilled surgeon may be effective in patients that have had recent device implantation, especially if prior to mediastinal healing.¹⁶ If external defibrillation/cardioversion is required, the percutaneous lead should not be disconnected from the system controller and the pump should not be stopped prior to the delivery of a shock.¹⁷

Study Limitations

This was a retrospective study and has the limitations common to all such studies. It is possible that some of the patients in our study sought care at a hospital ED outside of our system, and therefore were not included in our study. This, however, is exceedingly unlikely as the cardiologists and care team continually emphasized and instructed all patients in our study only to present to the study hospital ED for any complaint. Similarly, the various emergency medical services agencies for our region were also instructed to bring all LVAD patients to the study hospital.

Another limitation of our study is the relatively small total number of patients (98) and that our findings may not apply to other patient populations. This limitation, however, would be true for any hospital system that limits the type of LVAD implant procedure to one manufacturer (HMII in this instance).

Conclusion

Emergency physicians must be prepared to evaluate the LVAD patient presenting to the ED. A little over 55% of the time, the visit will be directly related to the LVAD; in the remainder of cases, patient presentation will be due to a non-LVAD-related cause. At initial presentation, however, the EP should assume that the ED visit is related to the LVAD, until a thorough history and physical examination can exclude otherwise.

Because of the high incidence of GI bleeding in LVAD patients, a rectal examination for blood in the stool should be performed for any complaint that may be related, such as generalized weakness, syncope, or shortness of breath. In the majority of cases, a complete blood count; complete metabolic profile, including lactic acid dehydrogenase; and coagulation studies, including prothrombin time and INRs, are indicated. Most patients with an LVAD will require a member of the VAD team (typically the perfusionist or biomedical engineer) to interrogate the controller if there is any concern about its function, including alarm sounding or lights flashing.

References

1. Benjamin EJ, Blaha MJ, Chiuve SE, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2017 update: a report from the American Heart Association. Circulation. 2017;135(10):e146-e603. doi:10.1161/CIR.0000000000000485. Erratum in: Circulation. 2017;135(1):e646. doi:10.1161/CIR.0000000000000491.

2. Lund LH, Edwards LB, Kucheryavaya AY, et al. The Registry of the International Society for Heart and Lung Transplantation: thirtieth official adult heart transplant report—2013; focus theme: age. J Heart Lung Transplant. 2013;32(10):951-964. doi:10.1016/j.healun.2013.08.006.

3. UNOS (United Network for Organ Sharing) Web site. https://unos.org/data/transplant-trends/waiting-list-candidates-by-organ-type/. Accessed February 8, 2018.

4. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017;36(10):1080-1086. doi:10.1016/j.healun.2017.07.005.

5. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251. doi:10.1056/NEJMoa0909938.

6. Kirklin JK, Naftel DC, Pagani FD, et al. Seventh INTERMACS annual report: 15,000 patients and counting. J Heart Lung Transplant. 2015;34(12):1495-1504. doi:10.1016/j.healun.2015.10.003.

7. Ambardekar AV, Buttrick PM. Reverse remodeling with left ventricular assist devices: a review of clinical, cellular and molecular effects. Circ Heart Fail. 2011;4(2):224-233. doi:10.1161/CIRCHEARTFAILURE.110.959684.

8. Slaughter MS, Pagani FD, Rogers JG, et al. Clinical management of continuous-flow left ventricular assist devices in advanced heart failure. J Heart Lung Transplant. 2010;29 (suppl 4):1-39. doi:10.1016/j.healun.2010.01.011.

9. Lo BM, Devine AS. Patients with left ventricular assist devices. Critical Decisions in Emergency Medicine. 2014;28(7):2-9.

10. Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation guidelines for mechanical circulatory support: executive summary. J Heart Lung Transplant. 2013;32(2):157-187. doi:10.1016/j.healun.2012.09.013.

11. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart transplantation. N Engl J Med. 2007;357(9):885-896. doi:10.1056/NEJMoa067758.

12. McIlvennan CK, Magid KH, Ambardekar AV, et al. Clinical outcomes following continuous-flow left ventricular assist device: a systematic review. Circ Heart Fail. 2014;7(6):1003-1013. doi:10.1161/Circheartfailure.114.001391.

13. Mulloy DP, Bhamidipati CM, Stone ML, et al. Cryoablation during left ventricular assist device implantation reduces postoperative ventricular tachyarrhythmias. J Thorac Cardiovasc Surg. 2013;145(5):1207-1213. doi:10.1016/j.jtcvs.2012.03.061.

14. Stern DR, Kazam J, Edwards P, et al. Increased incidence of gastrointestinal bleeding following implantation of the Heartmate II LVAD. J Card Surg. 2010;25(3):352-356. doi:10.1111/j.1540-8191.2010.01025.x.

15. Draper KV, Huang RJ, Gerson LB. GI bleeding in patients with continuous-flow left ventricular assist devices: a systematic review and meta-analysis. Gastrointest Endosc. 2014;80(3):435-446. doi:10.1016/j.gie.2014.03.040.

16. Aissaoui N, Morshuis M, Diebold B, et al. Heart failure while on ventricular assist device support: a true clinical entity? Arch Cardiovasc Dis. 2013:106(1):44-51. doi:10.1016/j.acvd.2012.09.006.

17. Thoratec HeartMate II Left Ventricular Assist System (LVAS) Information and Emergency Assistance Guide. Thoratec Corporation Web site. http://www.thoratec.com/_assets/download-tracker/HM_II_Info_Emergency_Assist_Guide_US_103873B_ENGLISH.pdf. Accessed July 5, 2017.

18. Peberdy MA, Gluck JA, Ornato JP, et al; American Heart Association Emergency Cardiovascular Care Committee; Council on Cardiopulmonary, Critical Care, Perioperative, and Resuscitation; Council on Cardiovascular Diseases in the Young; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support a scientific statement from the American Heart Association. Circulation. 2017;135(24):e1115-e1134. doi:10.1161/CIR.0000000000000504.

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Author and Disclosure Information

Authors’ Disclosure Statement: Dr Herre reports that he is a coinvestigator for the Multicenter Study of MagLev Technology in Patients Undergoing Mechanical Circulatory Support Therapy With HeartMate 3 (MOMENTUM 3) trial. The other authors report no actual or potential conflict of interest in relation to this article.

Dr Devine is an assistant professor in the department of emergency medicine, Eastern Virginia Medical School; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Knapp is a professor and residency program director, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Lo is an associate professor, emergency medicine residency program, Eastern Virginia Medical School, Norfolk; medical director, Sentara Norfolk General Hospital, Virginia; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Bono is a professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Harbin is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Jennings is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Gogel is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk. Dr Johnson is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk. Dr Bernstein is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Dr Alimard is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Dr Old is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Ms Hoedt Sentara Cardiology Specialists, Norfolk, Virginia. Dr Herre is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia.

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This article is adapted from preliminary data presented at the 2012 American College of Emergency Physicians’ Research Forum.

Introduction

Left Ventricular Assist Devices

HeartMate II Patient ED Presentation Study

Purpose

Our study involved only patients implanted with the HMII LVAD.

Methods

Patients and Study Design

Results

Discussion

Device Designs and Structures

Anticoagulation Therapy

Cardiopulmonary Evaluation

Bleeding

Volume Overload

Weakness, Lightheadedness, Dizziness, Syncope

Device Malfunction

Neurological Events

Cardiac Events and Management

Study Limitations

Conclusion

Introduction

Left Ventricular Assist Devices

HeartMate II Patient ED Presentation Study

Purpose

Our study involved only patients implanted with the HMII LVAD.

Methods

Patients and Study Design

Results

Discussion

Device Designs and Structures

Anticoagulation Therapy

Cardiopulmonary Evaluation

Bleeding

Volume Overload

Weakness, Lightheadedness, Dizziness, Syncope

Device Malfunction

Neurological Events

Cardiac Events and Management

Study Limitations

Conclusion

References

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Emergency Medicine - 50(2)

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Emergency Medicine - 50(2)

Page Number

49-56

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49-56

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Emergency Medicine

MDedge Emergency Medicine

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MDedge Emergency Medicine

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Cardiology

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Article

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Bites and Stings

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Bites and Stings

Author(s)

Katy Deljoui, MD

Barry J. Knapp, MD

Venomous bites and stings are responsible for significant mortality and morbidity worldwide.¹ Interestingly, arthropods account for a higher percentage of deaths from envenomation than snakes, usually due to allergic reactions.² In 2012, the American Association of Poison Control Centers (AAPCC) counted over 64,000 cases of bites and envenomations, some of which resulted in severe reactions.³ Fatalities from such exposures are typically rare, but severe systemic allergic reactions can occur. It is estimated that the incidence of anaphylaxis is approximately 50 to 2,000 episodes per 100,000 persons or a lifetime prevalence of 0.05% to 2.0%.⁴ Fortunately, most reactions are mild and only require supportive treatment. Envenomation and associated reactions, however, can present to the ED as life-threatening situations.⁵ Therefore, it is essential that the emergency physician (EP) be competent in the evaluation and treatment of a wide array of bites and stings.

Hymenoptera

The order Hymenoptera of the phylum Arthropoda can be divided into three subgroups that are medically relevant: (1) Apidae (Apids), which include the honeybee and bumblebee; (2) Vespidae, (Vespids) which include yellow jackets, hornets and wasps; and (3) Formicidae (ants).⁶

Bees and Wasps

Honeybees and bumblebees are rather docile and will not sting unless provoked. Only female bees are capable of stinging and are only able to do so once. Their stinging apparatus originates in the abdomen and consists of a sac containing venom that is attached to a barbed stinger (Figure 1). During an attack, the sac contracts, depositing venom into the victim’s tissue; the stinging apparatus then detaches from the insect’s body, eventually causing its death. In contrast, yellow jackets, hornets, and wasps have a different stinging apparatus that can be withdrawn from the victim after an attack. Thus, these insects can inflict multiple stings and still survive.

The main allergens in Apid venom are phospholipase A2, hyaluronidase, and melittin. Melittin, the main component, is a membrane active polypeptide that causes degranulation of basophils and mast cells. The allergens in Vespid venom are phospholipase, hyaluronidase, and antigen 5. As all Hymenoptera share some of these components, cross-sensitization may occur and individuals may be allergic to more than one species.⁷

The typical reaction to an insect sting is localized pain, swelling, and erythema; these symptoms generally subside after several hours. Little treatment is required other than analgesics and cold compresses. More extensive local reactions are also common, with swelling extending from the sting site over a large area.⁸ Symptoms typically peak within 48 hours and last as long as 7 days. The usual recommended treatment is nonsteroidal anti-inflammatory drugs (NSAIDs) (400-800 mg every 6-8 hours) and/or antihistamines (eg, diphenhydramine 50 mg orally every 6 hours as needed). Systemic steroids such as prednisone (40 mg orally daily for 2-3 days) are also beneficial and may be considered.2 Individuals exhibiting impressive localized reactions to stings tend to have similar responses after subsequent stings. The risk of anaphylaxis is approximately 5% per episode.⁹

Occasionally after multiple stings, patients present with symptoms of a systemic toxic reaction. This is often seen in an Africanized bee attack. These so-called “killer bees” are hybrids of African bees that escaped from laboratories in Brazil in the 1950s and spread northward; they are found in most of the warmer US states. Their venom is not more toxic than that of any other bee, but Africanized honeybees are more aggressive and respond to a perceived threat in far greater numbers. The reaction that results from multiple stings is systemic and may resemble anaphylaxis. Common symptoms include nausea, vomiting, and diarrhea, as well as lightheadedness and syncope. Interestingly, urticaria and bronchospasm are not universally present, even though respiratory failure and cardiac arrest may occur. Other symptoms include renal failure with acute tubular necrosis, myoglobinuria or hemoglobinuria, hepatic failure, and disseminated intravascular coagulation (DIC).^10,11 In addition, there have been reports of unusual reactions such as vasculitis, nephrosis, neuritis, encephalitis, and serum sickness. Late-appearing symptoms usually start several days to weeks after a sting and tend last for a prolonged period of time. Serum sickness tends to appear 5 to 14 days after exposure and consists of fever, malaise, headache, urticaria, lymphadenopathy, and polyarthritis.¹² Of note, patients who have venom-induced serum sickness may be at risk for anaphylaxis after subsequent stings and may therefore be suitable candidates for venom immunotherapy.¹³

Anaphylaxis

The definition of anaphylaxis is not universally agreed upon. The American Academy of Allergy, Asthma and Immunology defines anaphylaxis as a serious allergic response that often involves swelling, hives, hypotension and, in severe cases, shock. A major difference between anaphylaxis and other allergic reactions is that anaphylaxis typically involves more than one body system.¹⁴ The clinical features of anaphylaxis from insect stings are the same as those from other causes, typically generalized urticaria, facial flushing, and angioedema. Abdominal cramping, nausea, vomiting, and diarrhea are also seen. Life-threatening symptoms include stridor, circulatory collapse with shock, and bronchospasm. Symptoms usually begin 10 to 20 minutes after a sting, and almost all will develop within 6 hours. Interestingly, symptoms may recur 8 to 12 hours after the initial reaction.^15-18

Management

Immediate removal of the bee stinger is the most important principle as it precludes any further venom transfer. Traditional teaching recommended scraping the stinger out to avoid squeezing remaining venom into the tissues; however, involuntary muscle contractions of the gland continue after the stinger detaches, and the venom is quickly exhausted. Thus, immediate removal of the stinger is crucial, though the method of removal is now thought irrelevant.¹⁹

The sting site should be washed with soap and water to minimize chance of infection. Intermittent application of an ice pack may decrease edema and possibly prevent further absorption of the venom. Nonsteroidal anti-inflammatory drugs can be used to relieve pain. Although rarely necessary, standard doses of opioids may also be administered.

The mainstay of therapy for serious reactions is intramuscular (IM) epinephrine. The initial dosing is 0.3 to 0.5 mg (0.3 to 0.5 mL of 1:1000 concentration) in adults, and 0.01 mg/kg in children (maximum 0.3 mg). The injection should be IM and not subcutaneous, as IM dosing provides higher and more consistent and rapid peak blood epinephrine levels.²⁰ Concomitant intravenous (IV) administration of standard antihistamines, often diphenhydramine 1 mg/kg (generally 25-50 mg) and histamine-2 receptor antagonists (typically ranitidine 50 mg) are also recommended. The administration of steroids (methylprednisolone 125 mg IV or prednisone 60 mg orally) is traditionally recommended and thought to help potentiate the effect of other interventional measures.20 Bronchospasm, if present, is treated with nebulized β-agonists (albuterol). Hypotension may develop and requires significant crystalloid infusion—often several liters. If hypotension persists despite adequate fluid replacement, vasopressor therapy is recommended.

If a patient does not respond to initial treatment and cardiovascular (CV) collapse is evident, IV infusion of epinephrine should be initiated. Epinephrine, 100 mcg (0.1 mg) IV, should be given as a 1:100,000 dilution. This can be done by placing epinephrine, 0.1 mg (0.1 mL of the 1:1000 dilution), in 10 mL of normal saline solution and infusing it over 5 to 10 minutes (a rate of 1 to 2 mL/min). If the patient is refractory to the initial bolus, then an epinephrine infusion can be started by placing epinephrine, 1 mg (1.0 mL of the 1:1000 dilution), in 500 mL of 5% dextrose in water or NS and administering at a rate of 1 to 4 mcg per minute (0.5 to 2 mL/min), titrating to effect.²⁰ Antivenins have been studied for treatment, but none are commercially available at this time.²¹ Patients with anaphylaxis associated with severe signs and symptoms, including any evidence of CV collapse, should be admitted to the hospital for aggressive therapy and monitoring. Persons with mild-to-moderate reactions should be observed for 4 to 6 hours to monitor for late occurring symptoms. Outpatient therapy with antihistamines, oral steroids, and a prescription for an epinephrine auto-injector—including training on proper administration prior to discharge—are strongly recommended.²² Follow-up with an allergist is also indicated in patients with significant reactions, as skin testing and immunotherapy may be beneficial to prevent anaphylaxis during future exposures.

Ants

There are five species of fire ants in the United States, three native and two imported species (Figure 2). The imported species entered the United States in the 1930s and have since become well established in the Gulf region and in the Southwest.²³ They typically inhabit loose dirt and are characterized by their tendency to swarm when provoked. Fire ants generally attack in great numbers, cover the victim in a swarm, and sting simultaneously in response to a pheromone released by one or multiple individuals.

Fire ant venom is composed of an insoluble alkaloid, and crossreactivity with the venom of other Hymenopteras species does exist. Stings generally result in a papule, which evolves into a sterile pustule. Localized necrosis, scarring, and secondary infection can occur. Systemic reactions with angioedema and urticaria have been documented, which can sometimes lead to fatalities.²⁴

Treatment
Treatment of fire ant stings begin and end with local wound care. If the reaction is systemic, a treatment plan similar to that outlined in the treatment section for bees and wasps is indicated.

Araneae

The order Araneae of the phylum Arthropoda includes over 34,000 species of spiders divided into 105 families. Of those, only half a dozen are medically relevant and only three are commonly encountered in the United States. These include Loxosceles (most notably, the brown recluse spider), Tegeneria (mainly the hobo brown spider) and Latrodectus (includes the black widow spider). True spiders have a worldwide distribution and tend to thrive in heavily populated areas, resulting in many biting episodes per year. Data from the AAPPC’s most recent annual report listed 9,255 single spider-bite exposures in 2012, with one associated death.³

Spiders are carnivores and use venom to paralyze their prey. They are generally not a threat to humans as their fangs are too small to penetrate human skin, and the amount of venom injected is too small to produce toxicity. Thus, reactions resulting from a spider bite are typically limited to a localized reaction. Fortunately, most bites only require supportive medical therapy.

Loxosceles

Loxosceles are present worldwide, but L reclusa (the “brown recluse spider”) accounts for a significant number of envenomations in the United States. The AAPCC’s 2012 data notes 1,365 cases of exposure to the brown recluse spider with 510 of those victims seeking medical care.³ In many instances, clinicians attribute necrotic bites to the brown recluse spider, however, confirmation is often lacking. Loxosceles are nocturnal, and they are found both indoors and outdoors—mostly in dark and dry areas such as basements, closets, and woodpiles. These spiders are shy, but may bite when threatened. Their venom contains enzymes, including hyaluronidase and sphingomyelinase. Though rare, wounds can become necrotic due to neutrophil activation, platelet aggregation, and thrombosis.²⁵ The most common reaction to a Loxosceles bite is a mild painless erythematous lesion that becomes firm and generally heals over several days to weeks. In severe reactions, erythema, edema, and pruritus initially develop, followed within 24 to 72 hours by a hemorrhagic bulla surrounded by blanched skin. This leads to the “red, white, and blue sign” (ie, erythema, blanching, and ecchymosis). Infrequently, the ecchymotic area becomes necrotic and ulcerates in 3 to 5 days. The differential diagnoses should include necrotizing fasciitis, erythema chronicum migrans (from Borrelia-infected tick bites), and anthrax. Ulcerated lesions may result in significant cosmetic defect. Healing may take up to 2 weeks, and skin grafting is occasionally required.²⁶

Systemic effects are rare and usually develop in children between 24 to 72 hours after a bite. These include hemolysis, thrombocytopenia, hemoglobinuria, rhabdomyolysis, renal failure, DIC, nausea, vomiting, fever, and chills. Although common after bites of L laeta (the predominant South American species), these presentations are exceedingly infrequent in bites from the brown recluse seen in the United States. In the appropriate clinical context, a complete blood count, blood urea nitrogen/creatinine ratio, and coagulation profile may be considered.

Treatment begins with the usual supportive measures, including analgesia, ice, elevation, and a light compression dressing. Antibiotics are not indicated, unless there are signs of secondary infection. Serial evaluation for wound checks should be arranged. If ulceration develops, surgical debridement may be required. The vast majority of bites heal with supportive care alone, and aggressive medical therapy is usually not warranted.²⁷Patients with systemic manifestations should be admitted to the hospital for further care. There is no evidence-based literature to guide therapy. Many therapies have been tried with variable results and there remains no definitive standard of care.

Treatment regimens include antihistamines, antivenin, colchicine, dapsone, hyperbaric oxygen, cyproheptadine, surgical excision, and steroids.²⁸ Dapsone continues to be widely advocated worldwide despite its known adverse effects—most notably hemolysis and methemoglobinemia. Antivenin administration has shown some promise in animal models, but its efficacy in humans is still unclear.²⁹

Tegenaria

The Tegenaria agrestis or hobo spider is a native of Europe and central Asia and is only found in the northwest part of the United States. It is considered aggressive and tends to bite even with only mild provocation. The clinical presentation, inclusive of systemic reactions, is similar to that of the brown recluse spider. Similarly, there is no proven treatment. Surgical wound resection and skin grafting should be considered and is at times required.

Latrodectus.

Latrodectus, also known as widow spiders, are found worldwide. Five species are commonly found in the United States, but the black widow is the most well known. Only three of the species are actually black. Other varieties are typically brown or red. However, almost all Latrodectus spiders have a characteristic orange-red hourglass-shaped marking (Figure 3). Widow spiders aggressively defend their webs, and are most often found in woodpiles, basements, garages, and sheds. Most bites occur in the warmer months, between April and October.

The venom of the black widow spider contains mostly β-latrotoxin, which acts through both calcium-dependent and independent pathways and ultimately leads to the release of acetylcholine and norepinephrine neurotransmitters.³⁰ The bite of a widow spider is typically felt immediately as a pinprick sensation, followed by the development of pain 20 to 60 minutes later. In most cases, a small macule then appears at the bite site, which may evolve into a larger target lesion with a blanched center and surrounding erythema. Patients often complain of muscle cramp-like spasms. Severe abdominal wall musculature pain is a classic presentation and can create enough rigidity to simulate peritonitis on examination. Pain and muscle spasm can be controlled with opioids and benzodiazepines. Although IV calcium has been advocated to relieve symptoms, this therapy has shown no clear benefits and supporting research is lacking.³¹ Other rarely reported complications include atrial fibrillation, myocarditis, priapism, and death. In the vast majority of cases, recovery is excellent and occurs in 3 to 7 days

Latrodectus antivenin is very effective, often resolving symptoms rapidly and reducing the duration of illness—even when administered up to 90 hours postenvenomation.³² This antivenin is derived from horse serum, and hypersensitivity reactions are possible. One death from anaphylaxis has been reported in the United States after antivenin was given undiluted via IV push; however, slow administration of diluted antivenin is considered safe.³³

Diptera

The order Diptera of the phylum Arthropoda includes over 240,000 species. Among those, the mosquitoes and flies are the most medically relevant.

Mosquitoes
An actual mosquito bite itself causes minimal trauma and is not usually felt by the victim. However, the local anesthetic that is injected into the wound at the time of the attack causes local tissue damage. Mosquito bites can lead to both immediate and delayed reactions. Typical immediate reactions are of short duration and include edema, erythema, and pruritus. More severe reactions are extremely rare and consist of skin necrosis. Delayed skin reactions are fairly common, but tend to last longer, persisting for days or even weeks. Treatment is symptomatic, usually with antihistamines and NSAIDS.

Patients can acquire an allergy to mosquito saliva over time and develop increasingly pronounced edematous and pruritic lesions with subsequent bites. They can also experience fever, malaise, generalized edema, as well as severe nausea and vomiting.

Systemic or anaphylactic reactions are not known to occur. Instead, the greatest danger occurs with the transmission of life-threatening diseases. Malaria, yellow fever, dengue hemorrhagic fever, and different types of equine encephalitis are all transmitted by mosquito bites. One interesting newcomer to the United States is the West Nile virus (WNV), which has spread rapidly since its introduction in 2003. Over 1,850 cases were reported in 22 different states over the initial 8 months. Acute symptoms are mild in the majority of patients, but a small minority can experience fatal disease. Neurological symptoms include tumor, myoclonus, and Parkinsonism. An irreversible poliomyelitis-like syndrome may also develop. In addition to WNV, St Louis encephalitis and equine encephalitis also remain important pathogens in the United States.³⁴ Prevention of bites is crucial and includes the use of pyrethroid-impregnated mosquito netting, repellents, and oral malaria prophylaxis. N,N-diethyl-3-methylbenzamide (DEET) remains the most effective mosquito repellent.³⁵ Although toxic reactions are rare, they do occur and anaphylaxis has been reported. ^36,37

Flies
Flies are blood-sucking insects that feed by stabbing and piercing their victim’s skin. Their bites always cause some degree of pain and pruritus. Allergic reactions are possible, though not as severe as those produced by Hymenoptera venom. Treatment is largely symptomatic with ice, oral antihistamine, analgesics. and topical or oral steroids as needed. Secondary bite infection is a concern and antibiotics are sometimes necessary.

Shiponaptera

The order Shinoptera includes fleas and lice. All produce very similar lesions, making diagnosis difficult. One concern with these bites is the development of secondary infections, especially in children. The skin should be washed with soap and water. Calamine, cool soaks, and oral or topical antihistamine may all be helpful to reduce symptoms.

Fleas
With fleas, as with mosquitoes, there is additionally a concern for transmission of life-threatening diseases. Fleas transmit bubonic plague, endemic typhus, brucellosis, melioidosis, and erysipeloid. Fortunately, effective oral and injectable formulations for both dogs and cats are now available to control fleas on most family pets.

Lice

Head (Figure 4) and pubic lice have not been proven to transmit life-threatening diseases, though body lice remains an important disease vector. Body lice thrive in conditions of poverty. Studies among the homeless in industrialized countries have shown that Bartonella organisms can be transmitted by body lice and can cause endocarditis.^38,39 Furthermore, body lice remain important vectors for relapsing fever, trench fever, and epidemic typhus in refugee and war camps. In those settings, surveillance of lice for the presence of diseases has correctly predicted outbreaks of disease.⁴⁰

Hemiptera

The order Hemiptera includes two families that are medically relevant: the Reduviidae (“kissing bugs”) and Cimicidae (bed bugs; Figure 5). Found worldwide, both are blood-sucking arthropods and primarily nocturnal feeders that tend to hide in cracks and crevices near beds. Bites are typically painless and may result in erythematous papules, bullae, or wheals. Bed bug bites appear as erythematous papules, generally clustered and often linear. Kissing bug bites are not linear and are generally not accompanied by brown or black patterns of excrements on the bed linen—a distinctive characteristic of bed bugs.⁴¹ Treatment is largely supportive with patients often benefiting from local wound care and the use of topical corticosteroids.⁴²

Lepidoptera

The order Lepidoptera includes butterflies and moths and their caterpillars. Symptoms that result from contact with this class of insects are referred to as lepidopterism. Caterpillars have hair or spines for protection, which are also sometimes connected to a venom gland. Contact with these spines usually causes localized skin irritation and pruritus. Megalopyge opercularis, also known as the “puss caterpillar,” is mainly found in the southeastern United States and accounts for the majority of envenomation cases in this country. Intense local burning pain is typical at the site of contact and is followed by a grid-like pattern of hemorrhagic papules, which appear 2 to 3 hours after exposure and may last for several days. Regional lymphadenopathy is common. Other symptoms include headache, fever, hypotension, and convulsions. No deaths have ever been reported.

As there is no antivenin available for lepidopterism, treatment is mostly supportive. If spines are visible following contact, they should be removed with adhesive tape. Antihistamines and steroids may be used for symptom control. In patients with hypotension, IV fluids and IV epinephrine may be required.⁴³

Coleoptera

The order Coleoptera includes a large number of beetles, though clinically significant envenomation occurs only with blister beetles. There are over 1,500 species of blister beetles worldwide, approximately 2,002 of which are in the United States. The blister beetle responsible for most of the medically significant envenomations is Cantharis vesicatoria—also known as “Spanish fly.” Of note, the Spanish fly is not naturally found in the United States.

The venom of blister beetles contains a vesicant called cantharidin, which is exuded from their body when crushed. For this reason, a blister beetle should be removed by blowing or flicking. When contact with the poison does occur, it may lead to local inflammation and bullae formation.

Cantharidin-containing substances are sometimes used medicinally in wart removal preparations and are also sold for their purported aphrodisiac effects (the associated vascular congestion and urethral inflammation are interpreted as enhanced sexuality). Transdermal absorption or ingestion may lead to systemic toxicity with severe vomiting, hematemesis, abdominal pain, diarrhea, hematuria, renal failure, etc. Death has been reported after large ingestions.

Treatment is largely supportive. The skin should be irrigated thoroughly after exposure, followed by local wound care. Patients who present after ingestion should be admitted to the hospital for further treatment and care.⁴⁷

Conclusion

Knowledge of a vast array of stinging insects and spiders is important for any clinician, but the appropriate evaluation and treatment of bites and envenomations are crucial for EPs. Most exposures can be treated with supportive care, while others require in-depth knowledge and clinical expertise.

Dr Deljoui is a former resident, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and current critical care fellow, University of Maryland, Baltimore.

Dr Knapp is an associate professor and residency program director, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

References

White J. Bites and stings from venomous animals: a global overview. The Drug Monit. 2000;22(1):65-68.
Oten EJ. Venomous animal injuries. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Vol 1. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014:794-807.
Mowry JB, Spyker DA, Cantilena LR Jr, Bailey JE, Ford M. 2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report. Clin Toxicol (Phila). 2013;51(10):949-1229. doi:10.3109/15563650.2013.863906. https://aapcc.s3.amazonaws.com/pdfs/annual_reports/2012_NPDS_Annual_Report.pdf. Accessed April 2, 2014.
Liberman P, Camargo CA, Bohike K, et al. Epidemiology of anaphylaxis: findings of the American College of Allergy, Asthma and Immunology Epidemiology of Anaphylaxis Working Group. Ann Allergy Asthma Immunol. 2006;97(5):596-602.
Barnard JH. Studies of 400 Hymenoptera sting deaths in the United States. J Allergy Clin Immunol. 1973;52(5):259-264.
Frazier CA. Insect Allergy: Allergic and Toxic Reactions to Insects and Other Arthropods. 2nd Ed. St Louis, MO: WH Green; 1987:421.
King TP, Spangfort MD. Structure and biology of stinging insect venom allergens. Int Arch Allergy Immunol. 2000;123(2):99-106.
Antonicelli L, Bilo MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol.2002;2(4);341-346.
Mauriello PM, Barde SH. Natural history of large local reactions from stinging insects. J Allergy Clin Immunol. 1984;74(4 Pt 1):494-498.
Díaz-Sánchez CL, Lifshitz-Guinzberg A, Ignacio-Ibarra G, Halabe-Cherem J, Quinones-Galvan A. Survival after massive (>2,000) Africanized honey bee stings. Arch Intern Med. 1998;158(8):925-927.
Elston DM. Life-threatening stings, bites, infestations and parasitic diseases. Clin Dermatol. 2005;23(2):164-170.
Lazoglu AH1, Boglioli LR, Taff ML, Rosenbluth M, Macris NT. Serum sickness reaction following multiple insect stings. Ann Allergy Asthma Immunol. 1995;75(6 Pt 1):522-524.
Reisman RE, Livingston A. Late-onset allergic reactions, including serum sickness, after insect stings. J Allergy Clin Immunol. 1989;84(3);331-337.
Anaphylaxis. American Academy of Allergy, Asthma & Immunology Web site. http://www.aaaai.org/conditions-and-treatments/conditions-a-to-zsearch/anaphylaxis.aspx. Accessed April 2, 2014.
Brown H, Benton HS. Allergy to the Hymenoptera. V. Clinical study of 400 patients. Arch Intern Med. 1970;125(4):665-669.
Frazier CA. Allergic reactions to insect stings: a review of 180 cases. South Med J. 1964;57;1023-1034.
Mueller HL. Further experiences with severe allergic reactions to insect stings. N Engl J Med. 1959;161:374-377.
Lockey RF, Turkeltaub PC, Baird-Warren IA, et al. The Hymenoptera venom study I, 1979-1982: demographics and history-sting data. J Allergy Clin Immunol. 1988;82(3 Pt 1):370-381.
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Rowe BH, Gaeta T. Anaphylaxis, acute allergic reactions, and angioedema. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011:chap 6;52-54.
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Sections

Author(s)

Author(s)

Author and Disclosure Information

Hymenoptera

Bees and Wasps

Anaphylaxis

Management

Ants

Araneae

Loxosceles

Tegenaria

Latrodectus.

Diptera

The order Diptera of the phylum Arthropoda includes over 240,000 species. Among those, the mosquitoes and flies are the most medically relevant.

Shiponaptera

Lice

Hemiptera

Lepidoptera

Coleoptera

Conclusion

Dr Deljoui is a former resident, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and current critical care fellow, University of Maryland, Baltimore.

Dr Knapp is an associate professor and residency program director, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

Hymenoptera

Bees and Wasps

Anaphylaxis

Management

Ants

Araneae

Loxosceles

Tegenaria

Latrodectus.

Diptera

The order Diptera of the phylum Arthropoda includes over 240,000 species. Among those, the mosquitoes and flies are the most medically relevant.

Shiponaptera

Lice

Hemiptera

Lepidoptera

Coleoptera

Conclusion

Dr Deljoui is a former resident, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and current critical care fellow, University of Maryland, Baltimore.

Dr Knapp is an associate professor and residency program director, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

References

White J. Bites and stings from venomous animals: a global overview. The Drug Monit. 2000;22(1):65-68.
Oten EJ. Venomous animal injuries. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Vol 1. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014:794-807.
Mowry JB, Spyker DA, Cantilena LR Jr, Bailey JE, Ford M. 2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report. Clin Toxicol (Phila). 2013;51(10):949-1229. doi:10.3109/15563650.2013.863906. https://aapcc.s3.amazonaws.com/pdfs/annual_reports/2012_NPDS_Annual_Report.pdf. Accessed April 2, 2014.
Liberman P, Camargo CA, Bohike K, et al. Epidemiology of anaphylaxis: findings of the American College of Allergy, Asthma and Immunology Epidemiology of Anaphylaxis Working Group. Ann Allergy Asthma Immunol. 2006;97(5):596-602.
Barnard JH. Studies of 400 Hymenoptera sting deaths in the United States. J Allergy Clin Immunol. 1973;52(5):259-264.
Frazier CA. Insect Allergy: Allergic and Toxic Reactions to Insects and Other Arthropods. 2nd Ed. St Louis, MO: WH Green; 1987:421.
King TP, Spangfort MD. Structure and biology of stinging insect venom allergens. Int Arch Allergy Immunol. 2000;123(2):99-106.
Antonicelli L, Bilo MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol.2002;2(4);341-346.
Mauriello PM, Barde SH. Natural history of large local reactions from stinging insects. J Allergy Clin Immunol. 1984;74(4 Pt 1):494-498.
Díaz-Sánchez CL, Lifshitz-Guinzberg A, Ignacio-Ibarra G, Halabe-Cherem J, Quinones-Galvan A. Survival after massive (>2,000) Africanized honey bee stings. Arch Intern Med. 1998;158(8):925-927.
Elston DM. Life-threatening stings, bites, infestations and parasitic diseases. Clin Dermatol. 2005;23(2):164-170.
Lazoglu AH1, Boglioli LR, Taff ML, Rosenbluth M, Macris NT. Serum sickness reaction following multiple insect stings. Ann Allergy Asthma Immunol. 1995;75(6 Pt 1):522-524.
Reisman RE, Livingston A. Late-onset allergic reactions, including serum sickness, after insect stings. J Allergy Clin Immunol. 1989;84(3);331-337.
Anaphylaxis. American Academy of Allergy, Asthma & Immunology Web site. http://www.aaaai.org/conditions-and-treatments/conditions-a-to-zsearch/anaphylaxis.aspx. Accessed April 2, 2014.
Brown H, Benton HS. Allergy to the Hymenoptera. V. Clinical study of 400 patients. Arch Intern Med. 1970;125(4):665-669.
Frazier CA. Allergic reactions to insect stings: a review of 180 cases. South Med J. 1964;57;1023-1034.
Mueller HL. Further experiences with severe allergic reactions to insect stings. N Engl J Med. 1959;161:374-377.
Lockey RF, Turkeltaub PC, Baird-Warren IA, et al. The Hymenoptera venom study I, 1979-1982: demographics and history-sting data. J Allergy Clin Immunol. 1988;82(3 Pt 1):370-381.
Schneir AB, Clark RF. Bites and stings. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011:chap120;585-596.
Rowe BH, Gaeta T. Anaphylaxis, acute allergic reactions, and angioedema. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011:chap 6;52-54.
Jones RG1, Corteling RL, Bhogal G, Landon J. A novel Fab-based antivenom for the treatment of mass bee attacks. Am J Trop Med Hyg. 1999;61(3):361-366.
National Institutes of Health, US Department of Health and Human Services, National Insitute of Allergy and Infectious Diseases. Guidelines for the Diagnosis and Management of Food Allergy in the United States. Summary of the NIAID-Sponsored Expert Panel Report. Bethesda, MD: National Institutes of Health; 2010. NIH Publication No. 11-7700. http://www.niaid.nih.gov/topics/foodAllergy/clinical/Documents/FAGuidelinesExecSummary.pdf. Accessed April 2, 2014.
Kemp SF, deShazo RD, Moffitt JE, Williams DF, Buhner WA 2nd. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105(4):683-691.
Fernández-Meléndez S, Miranda A, García-González JJ, Barber D, Lombardero M. Anaphylaxis caused by imported red fire ant stings in Málaga, Spain. J Investig Allergol Immunol. 2007;17(1):48,49.
Swanson DL. Bites of brown recluse spiders and suspected necrotic arachnidism. N Engl J Med. 2005;352(7):700-707.
Saucier JR. Arachnid envenomation. Emerg Med Clin North Am. 2004;22(2):405-422.
Wright SW, Wrenn KD, Murray L, Seger D. Clinical presentation and outcome of brown recluse spider bite. Ann Emerg Med. 1997;30(1):28-32.
Phillips S, Kohn M, Baker D, et al. Therapy of brown spider envenomation: a controlled trial of hyperbaric oxygen, dapsone, and cyproheptadine. Ann Emerg Med. 1995;25(3):363-368.
Pauli I, Puka J, Gubert IC, Minozzo JC. The efficacy of antivenom in loxoscelism treatment. Toxicon. 2006;48(2):123-127.
Ushkaryov YA, Volynski KE, Ashton AC. The multiple actions of black widow spider toxins and their selective use in neurosecretion studies. Toxicon. 2004;43(5):527-542.
Clark RF, Wethern-Kestner S, Vance MV, Gerkin R. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21(7):782-787.
O’Malley GF, Dart RC, Kuffner EF. Successful treatment of latrodectism with antivenom after 90 hours. N Engl J Med. 1999;340(8):657.
Clark RF. The safety and efficacy of antivenin Latrodectus mactans. J Toxicol Clin Toxicol. 2001;39(2):125-127.
Sejvar JJ, Haddad MB, Tierney BC. Neurologic manifestations and outcome of West Nile virus infection [published correction appears in JAMA. 2003;290(10):1318]. JAMA. 2003;290(4):511-515.
Brown M, Herbert AA. Insect repellents: an overview. J Am Acad Dermatol. 1997;36(2 Pt 1):243-249.
Fradin MS. Mosquitoes and mosquito repellents: a clinician’s quide. Ann Intern Med. 1998;128(11):931-940.
Miller JD. Anaphylaxis associated with insect repellent. N Engl J Med. 1982;307(21):1341,1342.
Spach DH, Kanter AS, Dougherty MJ, et al. Bartonella (Rochalimaea) quintana bacteremia in inner-city patients with chronic alcoholism. N Engl J Med. 1995;332(7): 424-428.
Jackson LA, Spach DH, Kippen DA, et al. Seroprevalence to Bartonella quintana among patients at a community clinic in downtown Seattle. J Infect Dis. 1996;173(4):1023-1026.
Sundnes KO. Epidemic of louse-borne relapsing fever in Ethiopia. Lancet. 1993;342(8881):1213-1215.
Vetter R. Kissing bugs (Triatoma) and the skin. Dermatol Online J. 2001;7(1):6. http://escholarship.org/uc/item/59k2m8wt. Accessed April 2, 2014.
Stucki A, Ludwig R. Images in clinical medicine. Bedbug bites. N Engl J Med. 2008; 359:10)1047.
Kuspis DA, Rawlins JE, Krenzelok EP. Human exposures to stinging caterpillars: Lophocampa caryae exposures. Am J Emerg Med. 2001;19(5):396-398.
Moed L, Shwayder TA, 0.Chang MW. Cantharidin revisited: a blistering defense of an ancient medicine. Arch Dermatol. 2001;137(10):1357-1360.

References

White J. Bites and stings from venomous animals: a global overview. The Drug Monit. 2000;22(1):65-68.
Oten EJ. Venomous animal injuries. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Vol 1. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014:794-807.
Mowry JB, Spyker DA, Cantilena LR Jr, Bailey JE, Ford M. 2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report. Clin Toxicol (Phila). 2013;51(10):949-1229. doi:10.3109/15563650.2013.863906. https://aapcc.s3.amazonaws.com/pdfs/annual_reports/2012_NPDS_Annual_Report.pdf. Accessed April 2, 2014.
Liberman P, Camargo CA, Bohike K, et al. Epidemiology of anaphylaxis: findings of the American College of Allergy, Asthma and Immunology Epidemiology of Anaphylaxis Working Group. Ann Allergy Asthma Immunol. 2006;97(5):596-602.
Barnard JH. Studies of 400 Hymenoptera sting deaths in the United States. J Allergy Clin Immunol. 1973;52(5):259-264.
Frazier CA. Insect Allergy: Allergic and Toxic Reactions to Insects and Other Arthropods. 2nd Ed. St Louis, MO: WH Green; 1987:421.
King TP, Spangfort MD. Structure and biology of stinging insect venom allergens. Int Arch Allergy Immunol. 2000;123(2):99-106.
Antonicelli L, Bilo MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol.2002;2(4);341-346.
Mauriello PM, Barde SH. Natural history of large local reactions from stinging insects. J Allergy Clin Immunol. 1984;74(4 Pt 1):494-498.
Díaz-Sánchez CL, Lifshitz-Guinzberg A, Ignacio-Ibarra G, Halabe-Cherem J, Quinones-Galvan A. Survival after massive (>2,000) Africanized honey bee stings. Arch Intern Med. 1998;158(8):925-927.
Elston DM. Life-threatening stings, bites, infestations and parasitic diseases. Clin Dermatol. 2005;23(2):164-170.
Lazoglu AH1, Boglioli LR, Taff ML, Rosenbluth M, Macris NT. Serum sickness reaction following multiple insect stings. Ann Allergy Asthma Immunol. 1995;75(6 Pt 1):522-524.
Reisman RE, Livingston A. Late-onset allergic reactions, including serum sickness, after insect stings. J Allergy Clin Immunol. 1989;84(3);331-337.
Anaphylaxis. American Academy of Allergy, Asthma & Immunology Web site. http://www.aaaai.org/conditions-and-treatments/conditions-a-to-zsearch/anaphylaxis.aspx. Accessed April 2, 2014.
Brown H, Benton HS. Allergy to the Hymenoptera. V. Clinical study of 400 patients. Arch Intern Med. 1970;125(4):665-669.
Frazier CA. Allergic reactions to insect stings: a review of 180 cases. South Med J. 1964;57;1023-1034.
Mueller HL. Further experiences with severe allergic reactions to insect stings. N Engl J Med. 1959;161:374-377.
Lockey RF, Turkeltaub PC, Baird-Warren IA, et al. The Hymenoptera venom study I, 1979-1982: demographics and history-sting data. J Allergy Clin Immunol. 1988;82(3 Pt 1):370-381.
Schneir AB, Clark RF. Bites and stings. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011:chap120;585-596.
Rowe BH, Gaeta T. Anaphylaxis, acute allergic reactions, and angioedema. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011:chap 6;52-54.
Jones RG1, Corteling RL, Bhogal G, Landon J. A novel Fab-based antivenom for the treatment of mass bee attacks. Am J Trop Med Hyg. 1999;61(3):361-366.
National Institutes of Health, US Department of Health and Human Services, National Insitute of Allergy and Infectious Diseases. Guidelines for the Diagnosis and Management of Food Allergy in the United States. Summary of the NIAID-Sponsored Expert Panel Report. Bethesda, MD: National Institutes of Health; 2010. NIH Publication No. 11-7700. http://www.niaid.nih.gov/topics/foodAllergy/clinical/Documents/FAGuidelinesExecSummary.pdf. Accessed April 2, 2014.
Kemp SF, deShazo RD, Moffitt JE, Williams DF, Buhner WA 2nd. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105(4):683-691.
Fernández-Meléndez S, Miranda A, García-González JJ, Barber D, Lombardero M. Anaphylaxis caused by imported red fire ant stings in Málaga, Spain. J Investig Allergol Immunol. 2007;17(1):48,49.
Swanson DL. Bites of brown recluse spiders and suspected necrotic arachnidism. N Engl J Med. 2005;352(7):700-707.
Saucier JR. Arachnid envenomation. Emerg Med Clin North Am. 2004;22(2):405-422.
Wright SW, Wrenn KD, Murray L, Seger D. Clinical presentation and outcome of brown recluse spider bite. Ann Emerg Med. 1997;30(1):28-32.
Phillips S, Kohn M, Baker D, et al. Therapy of brown spider envenomation: a controlled trial of hyperbaric oxygen, dapsone, and cyproheptadine. Ann Emerg Med. 1995;25(3):363-368.
Pauli I, Puka J, Gubert IC, Minozzo JC. The efficacy of antivenom in loxoscelism treatment. Toxicon. 2006;48(2):123-127.
Ushkaryov YA, Volynski KE, Ashton AC. The multiple actions of black widow spider toxins and their selective use in neurosecretion studies. Toxicon. 2004;43(5):527-542.
Clark RF, Wethern-Kestner S, Vance MV, Gerkin R. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21(7):782-787.
O’Malley GF, Dart RC, Kuffner EF. Successful treatment of latrodectism with antivenom after 90 hours. N Engl J Med. 1999;340(8):657.
Clark RF. The safety and efficacy of antivenin Latrodectus mactans. J Toxicol Clin Toxicol. 2001;39(2):125-127.
Sejvar JJ, Haddad MB, Tierney BC. Neurologic manifestations and outcome of West Nile virus infection [published correction appears in JAMA. 2003;290(10):1318]. JAMA. 2003;290(4):511-515.
Brown M, Herbert AA. Insect repellents: an overview. J Am Acad Dermatol. 1997;36(2 Pt 1):243-249.
Fradin MS. Mosquitoes and mosquito repellents: a clinician’s quide. Ann Intern Med. 1998;128(11):931-940.
Miller JD. Anaphylaxis associated with insect repellent. N Engl J Med. 1982;307(21):1341,1342.
Spach DH, Kanter AS, Dougherty MJ, et al. Bartonella (Rochalimaea) quintana bacteremia in inner-city patients with chronic alcoholism. N Engl J Med. 1995;332(7): 424-428.
Jackson LA, Spach DH, Kippen DA, et al. Seroprevalence to Bartonella quintana among patients at a community clinic in downtown Seattle. J Infect Dis. 1996;173(4):1023-1026.
Sundnes KO. Epidemic of louse-borne relapsing fever in Ethiopia. Lancet. 1993;342(8881):1213-1215.
Vetter R. Kissing bugs (Triatoma) and the skin. Dermatol Online J. 2001;7(1):6. http://escholarship.org/uc/item/59k2m8wt. Accessed April 2, 2014.
Stucki A, Ludwig R. Images in clinical medicine. Bedbug bites. N Engl J Med. 2008; 359:10)1047.
Kuspis DA, Rawlins JE, Krenzelok EP. Human exposures to stinging caterpillars: Lophocampa caryae exposures. Am J Emerg Med. 2001;19(5):396-398.
Moed L, Shwayder TA, 0.Chang MW. Cantharidin revisited: a blistering defense of an ancient medicine. Arch Dermatol. 2001;137(10):1357-1360.

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Bites and Stings

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Characteristics, Frequency, and Disposition of Patients With a HeartMate II Left Ventricular Assist Device Presenting to the ED

Introduction

Left Ventricular Assist Devices

HeartMate II Patient ED Presentation Study

Purpose

Methods

Patients and Study Design

Results

Discussion

Device Designs and Structures

Anticoagulation Therapy

Cardiopulmonary Evaluation

Bleeding

Volume Overload

Weakness, Lightheadedness, Dizziness, Syncope

Device Malfunction

Neurological Events

Cardiac Events and Management

Study Limitations

Conclusion

Introduction

Left Ventricular Assist Devices

HeartMate II Patient ED Presentation Study

Purpose

Methods

Patients and Study Design

Results

Discussion

Device Designs and Structures

Anticoagulation Therapy

Cardiopulmonary Evaluation

Bleeding

Volume Overload

Weakness, Lightheadedness, Dizziness, Syncope

Device Malfunction

Neurological Events

Cardiac Events and Management

Study Limitations

Conclusion

Introduction

Left Ventricular Assist Devices

HeartMate II Patient ED Presentation Study

Purpose

Methods

Patients and Study Design

Results

Discussion

Device Designs and Structures

Anticoagulation Therapy

Cardiopulmonary Evaluation

Bleeding

Volume Overload

Weakness, Lightheadedness, Dizziness, Syncope

Device Malfunction

Neurological Events

Cardiac Events and Management

Study Limitations

Conclusion

Bites and Stings

Hymenoptera

Anaphylaxis

Management

Ants

Araneae

Diptera

Shiponaptera

Hemiptera

Lepidoptera

Coleoptera

Hymenoptera

Anaphylaxis

Management

Ants

Araneae

Diptera

Shiponaptera

Hemiptera

Lepidoptera

Coleoptera