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Emergency Medicine News:
doi: 10.1097/01.EEM.0000357589.69932.27
Living with the LLSA

Time to PCI, Procedural Sedation in the ED, and Acute Chemical Emergencies

Lovato, Luis M. MD

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Author Credentials and Financial Disclosure:

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Dr. Lovato is an Associate Professor of Medicine at the David Geffen School of Medicine at the University of California at Los Angeles, the Director of Critical Care for the Department of Emergency Medicine at Olive View-UCLA Medical Center, and the LLSA Workshop Co-Director for the Olive View-UCLA National Conference on Advances in Emergency Medicine.

All faculty and staff in a position to control the content of this CME activity have disclosed that they have no financial relationships with, or financial interests in, any commercial companies pertaining to this educational activity.

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Learning Objectives:

After reading this article, the physician should be able to:

1. Discuss the pros and cons of two approaches to reperfusion in ST-segment elevation myocardial infarction and the importance that time plays when choosing one strategy over the other.

2. Describe the American College of Emergency Physicians' recommendations on the approach to procedural sedation and analgesia.

3. Summarize the signs and symptoms of acute chemical exposure, and categorize the exposure into one of four toxidromes.

Release Date: July 2009

Article from the 2009 LLSA Reading List

Time to Treatment in Primary Percutaneous Coronary Intervention

Nallamothu BK, et al

N Engl J Med

2007;357(16):1631

Multiple time-dependent interventions often begin simultaneously when a critical patient arrives in the ED. The stakes are especially high with ST-segment elevation myocardial infarction (STEMI). This article reviews the pros and cons of two approaches to STEMI therapy, fibrinolytic therapy, and primary percutaneous intervention (PCI) in the context of one of the most important variables — time.

We are all familiar with cardiology's favorite adage that “time equals myocardium.” The authors emphasize this point by reviewing the pathophysiology of myocardial necrosis, reminding us that with 100% occlusion, myocardial death is complete within six hours. Several factors may extend the time before irreversible injury sets in, including partial occlusion, episodes of transient reperfusion, collateral circulation, and ischemic preconditioning.

With this in mind, guidelines from multiple cardiology groups including the American College of Cardiology, the American Heart Association, and the European Society of Cardiology, recommend reperfusing STEMI patients via primary coronary intervention (PCI) in less than 90 minutes of initial presentation. The Health Quality Alliance adopted this goal as a core measure of quality care, yet many institutions have difficulty achieving that goal.

A major barrier is that on-site PCI is simply not available at many U.S. institutions. Theoretically, rapid transfer to a STEMI receiving center is an option, but many social, economic, and legal obstacles in the U.S. health care system prevent efficient interhospital transfers within goal door-to-balloon times.

Institutions that do have PCI often do not have an interventional team on-site during off hours either, increasing the likelihood of PCI delay for patients on nights or weekends. Strategies that seem to correlate best with reducing door-to-balloon times are having on-site cardiology 24 hours a day, instituting simplified single-call STEMI team activation, and having the emergency physician activate the cath lab.

Although PCI seems to result in better outcomes for STEMI than fibrinolytic therapy, it is important to remember that fibrinolytics still have several key advantages over PCI including lower overall cost, universal availability, and ease of administration. The authors recommend fibrinolytics for STEMI within 30 minutes of ED presentation as the definitive route to acute reperfusion when EPs anticipate that door-to-balloon times (for whatever reason) cannot occur in under 90 minutes.

Articles from the 2008 LLSA Reading List

Clinical Policy: Procedural Sedation and Analgesia in the Emergency Department

Godwin SA, et al

Ann Emerg Med

2005;45(2):177

Anxiety and pain are inherent in many common ED procedures, making procedural sedation and analgesia (PSA) a core skill-set for the front-line EP. The American College of Emergency Physicians assembled this comprehensive clinical policy to help ED providers stay up-to-date on the latest literature regarding PSA and to offer evidence-based guidelines to help solve common dilemmas surrounding the issue.

As with other clinical policies from ACEP, individual articles from the available literature are initially assessed for quality and strength of evidence. Selected articles are subsequently used to answer key clinical questions, with the final strength of each recommendation based on the pooled body of evidence.

The only Level A recommendation, based on high clinical certainty or overwhelming consensus evidence, is:

▪ Ketamine is safe for PSA in children.The Level B recommendations, based on moderate clinical certainty or strong consensus evidence, are:

▪ Use pulse oximetry for patients with significant comorbidities or at increased risk of hypoxia (airway issues, moderate, or deep sedation targeted).

▪ Propofol, fentanyl, and midazolam are safe for PSA.

▪ Titrate nondissociative agents to effect.The Level C recommendations, based on preliminary, inconclusive, or conflicting evidence or evidence that originates from a panel consensus, are:

▪ Qualified support staff should be available to provide continuous monitoring during moderate or deep sedation.

▪ Staff should be supervised by an EP or credentialed provider.

▪ A targeted history and physical should be performed to identify possible contraindications or anticipate problems.

▪ Providers should consider the timing and amount of recent food intake when targeting the level of sedation, but recent food intake is not a contraindication.

▪ Providers should have access to oxygen, suction, reversal agents, and advanced airway and resuscitation equipment.

▪ Staff should document vital signs, appearance, and ability to respond to verbal stimuli before, during, and after PSA.

▪ Pulse oximetry may not be necessary when consciousness is minimally depressed and verbal communication is monitored and maintained.

▪ Consider capnometry to provide early information about depressed ventilation.

▪ Etomidate is safe for PSA.

Acute Chemical Emergencies

Kales SN, et al

N Engl J Med

2004;350(8):800

Fortunately, acute chemical emergencies are not very common, but that also means many emergency physicians do not obtain much real-world experience for chemical exposures. This article reviews the approach to the chemically exposed patient and guides initial management by discussing four acute chemical toxidromes: asphyxiants, cholinesterase inhibitors, respiratory tract irritants, and vesicant and skin caustics. The goal is to guide initial therapy of the chemically exposed patient and better prepare the EP for a mass casualty incident.

Emergency responders are well trained to initiate early decontamination efforts in the field, but EPs should be prepared to do the same when chemical exposures are unrecognized by EMS providers or if less critically affected patients present on their own. Depending on patient stability, it is extremely important and effective in decreasing additional exposure to remove all clothing early in the presentation, copiously irrigate with water, and wash with soap and water. Once suspected, early consultation with a poison center is crucial.

Asphyxiants are classified into simple ones, such as methane, that displace oxygen from inspired air, and chemical ones, such as carbon monoxide, cyanide, and hydrogen sulfide, that interfere with oxygen transport and cellular respiration, and can cause toxicity even with normal oxygen saturations. Neurologic and cardiovascular symptoms dominate this toxidrome, and can range from mild headache and lethargy to syncope, seizure, confusion, ischemia, and death depending on the exposure. All suspected cases should be treated with high-flow oxygen, and hyperbaric oxygen therapy should be considered for severe exposures.

Carbon monoxide should be suspected in colder seasons, potentially with multiple victims coming from one family when a faulty heating system is the culprit. Rapid syncope is characteristic of exposure to cyanide (laboratory/industry exposures) or hydrogen sulfide (exposure to decaying organic matter). Both should be suspected when hypotension and lactic acidosis persist despite adequate arterial oxygenation. Thiosulfate and sodium nitrite are both antidotes for cyanide toxicity, but sodium nitrite should be reserved for severe cases because it induces methemoglobinemia, which can exacerbate tissue hypoxia.

Cholinesterase inhibitors are grouped into three categories: organophosphate pesticides (e.g., malathion), carbamate pesticides, and organophosphorous nerve agents (e.g., sarin, VX). These agents can be ingested, inhaled, and absorbed through the skin, posing a threat to rescuers or ED personnel if victims are not properly decontaminated. Cholinergic overstimulation results in multiple symptoms easily recalled with the mnemonic DUMBELS (diarrhea, urination, miosis, bronchorrhea, emesis, lacrimation, salivation). Nicotinic effects include weakness and fasiculations, and central overstimulation results in seizures and coma. High-dose atropine reverses muscarinic effects, and the dose is titrated to relieve pulmonary symptoms. Pralidoxime reactivates acetylcholinesterase (ACh) with clinical effects at all ACh receptors, but is only effective before the nonreversible “aging” of organophosphate-ACh complexes. Seizures should be treated with benzodiazepines.

Respiratory tract irritants include high-solubility irritants (e.g., tear gas, ammonia, hydrochloric acid, and hydrosulfuric acid), intermediate-solubility irritants (e.g., chlorine), and low-solubility irritants (e.g., phosgene, nitrogen dioxide). High-solubility agents are rapidly absorbed, causing predominately upper-tract symptoms and early warning signs of toxicity. Low-solubility agents are less acutely irritating, can be more difficult to recognize, are more likely to penetrate into the lower respiratory tract, and are more likely to result in delayed onset acute lung injury. In addition to decontamination, care is largely supportive.

The final category is vesicants or blistering agents (e.g., mustard) and skin caustics (e.g., hydrofluoric acid). Historically used in warfare, mustard is an alkylating agent rapidly absorbed through mucus membranes, but initial symptoms are delayed four to 12 hours. Early effects are most prominent in the skin and eyes, with delayed effects on the airway. Systemic effects also can occur, and hematopoietic suppression is associated with a poor outcome. Treatment is largely supportive and likely to involve multidisciplinary consultation depending on affected organ systems. Hydrofluoric acid exposure presents with delayed onset chemical burns and intense local pain. Therapy is directed at local and systemic hypocalcemia caused by the release of fluoride, which has a high affinity for calcium.

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CME Participation Instructions

To earn CME credit, you must read the article in Emergency Medicine News, and complete the quiz, answering at least 80 percent of the questions correctly. Mail the completed quiz with your check for $10 payable to the Lippincott Continuing Medical Education Institute, Inc., 770 Township Line Road, Suite 300, Yardley, PA 19067. Only the first entry will be considered for credit, and must be received by Lippincott Continuing Medical Education Institute, Inc., by July 31, 2010. Acknowledgement will be sent to you within six to eight weeks of participation.

Lippincott Continuing Medical Education Institute, Inc., is accredited by the Accreditation Council for Continuing Medical Education to provide medical education to physicians. Lippincott Continuing Medical Education Institute, Inc., designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activities.

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Mnemonic for Symptoms Caused by Cholinergic Overstimulation: DUMBELS

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Diarrhea

Urination

Miosis

Bronchorrhea

Emesis

Lacrimation

Salivation

© 2009 Lippincott Williams & Wilkins, Inc.

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