Almost 2.4 million human exposures were logged into the National Poison Data System (NPDS) in 2010, a slight decrease from the year before. Previously called the Toxic Exposure Surveillance System, NPDS has been compiling data since 1985, and this year reported on 1146 fatalities from toxic exposures. (See FastLinks.)
One of the most interesting parts of the annual report is the description of some of the more interesting or unusual fatal cases, everything from a patient who intentionally took 800 aspirin tablets to one who cut open and ate a fentanyl patch. Two in particular caught my eye, and the first one is especially important.
Case 1: A 37-year-old man came to the emergency department after being bitten by a spider on the right shin. He was in moderate distress on presentation, with a small area of erythema on his shin. His blood pressure was 159/74 mm Hg, heart rate was 103 bpm, his respiratory rate was 22 bpm, and oxygen saturation was 96% on room air. No diaphoresis or abdominal tenderness was found. The patient had a history of asthma, and was taking albuterol and fluticasone.
One hour after the spider bite, the patient developed diaphoresis and tightness around his shoulder muscles and pain in his back and chest. These symptoms did not respond to 30 mg ketorolac, 2 mg lorazepam, and 2 mg hydromorphone. The cause of the bite was thought to be a black widow spider (genus Latrodectus), so he was given a test dose of horse serum, and after having no reaction, received an intravenous infusion of black widow spider antivenin (2.5 mL in 50 mL normal saline).
Fifteen minutes after the infusion began, the patient complained of facial paresthesias and shortness of breath, and he then developed anaphylactic shock with respiratory distress progressing to cardiopulmonary arrest. After resuscitation and treatment with epinephrine, steroids, diphenhydramine, and naloxone, he suffered a second arrest but then appeared to be improving. Unfortunately, he went on to develop acute renal failure and rapidly progressing hypoxemia. He died 36 hours after presentation.
At the Essentials of Emergency Medicine conference this past November in San Francisco, Sean Nordt, MD, and William Mallon, MD, debated the use of antivenin for black widow spider bites. Dr. Nordt, an assistant professor of clinical emergency medicine and the director of toxicology at the University of Southern California's Keck School of Medicine, said the clinical effects of Latrodectus bites include autonomic disturbances (hypertension, tachycardia), priapism, diaphoresis, and intractable pain that can last 72 hours or more. Antivenin often resolves these symptoms quickly, avoiding potential hospital admission for pain control and loss of time at work or school.
Although no deaths have been reported from Latrodectus bites in the United States, one case of death was linked to antivenin administration. This 2010 case reported by NPDS is now the second. Dr. Nordt said the first reported fatal case involved multiple medical errors. The antivenin was given IV push (not by the recommended slow infusion) to a patient with multiple drug -allergies. Resuscitation efforts also were complicated by occurrence of a pneumothorax. Dr. Nordt concluded that the antivenin was safe.
Dr. Mallon, also an associate professor of clinical emergency medicine at Keck and the director of International Emergency Medicine at LAC+USC Medical Center, disagreed. He contended that symptoms could be controlled with adequate — often high — doses of an opiate analgesic and a benzodiazepine in the vast majority of cases. “You can't give piddling doses of benzos and opiates, and say they failed and use that as an excuse to bring potentially lethal anaphylaxis into the game. Give more benzos! Give more fentanyl!” he said. While occasional severe cases may justify using antivenin, Dr. Mallon said such cases were extremely rare.
Of course, there is a difference between the chance for an extremely bad outcome when the antivenin is used optimally and when it is used under actual clinical conditions. It is obvious that the use of antivenin was less than ideal in this case. By any reckoning, the doses of analgesics and benzodiazepines administered were indeed “piddling,” and the fact that the patient had a history of asthma should have given the physician pause. This is an unfortunate but important case.
Case 2: A 58-year-old chemical plant worker was brought to the emergency department after being sprayed in the face with phosgene gas. At triage, his pulse was 80 bpm, his respiratory rate was 26 bpm, and his blood pressure was 98/65 mm Hg. He was externally decontaminated, and received intravenous fluids. Several hours later, he became short of breath, tachypneic, and hypoxic (oxygen saturation 80%). His condition deteriorated with the onset of pulmonary edema and hypotension, and he died the next day despite treatment with intubation and mechanical ventilation, oxygen, bronchodilators, and pressors.
This case demonstrates the key three words to remember about phosgene — delayed pulmonary edema. Phosgene (COCl2) is a colorless gas with an odor said to resemble freshly cut grass or musty hay. (Note: If you detect this aroma, you are way too close.) When hydrolyzed, phosgene produces hydrochloric acid, and is classified as an irritant gas. Unlike highly soluble irritant gases such as ammonia, however, it has low solubility in water and possesses poor warning properties; that is, upper airway irritation may be minimal, and seriously exposed patients often present with only a mild cough or sore throat.
Onset of serious toxicity with dyspnea and hypoxia can be delayed for up to eight hours as the gas works its way down to the lower airway where it attacks the alveolar lining, causing pneumonitis and pulmonary edema. It can be a serious mistake to discharge patients exposed to phosgene from the emergency department after only several hours of observation even if they look well. The Centers for Disease Control and Prevention recommends that these patients be monitored for up to 48 hours to avoid missing delayed or recurrent toxicity.
Managing phosgene exposure starts with the basic ABCs and then careful, prolonged observation. Symptomatic patients can be treated with oxygen and nebulized beta-agonists as well as respiratory and circulatory support. Some authors suggest that clinicians should consider early intubation using an ARDSnet protective ventilation strategy. (Clin Toxicol 2010;48:497.)
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Dr. Gussowis a voluntary attending physician at the John H. Stroger Hospital of Cook County in Chicago (formerly Cook County Hospital), an assistant professor of emergency medicine at Rush Medical College, and a consultant to the Illinois Poison Center. He is also the editor of his own blog, The Poison Review (www.thepoisonreview.com).
- Read the 2010 NPDS report at http://bit.ly/zEfNq8.
- Visit Dr. Gussow's blog at www.thepoisonreview.com.
- Read all of Dr. Gussow's past columns in the EM-News.com archive.
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