incidence of complications in a group of carbon monoxide-intoxicated patients receiving hyperbaric oxygen therapy." We agree that such complications are secondary to the toxic effects of carbon monoxide, not due to the hyperbaric oxygen therapy. Carbon monoxide was the implied etiologic agent when we stated that "all of the cardiac arrests and myocardial infarctions and two of the three cases complicated by symptomatic myocardial ischemia occurred prior to hyperbaric oxygen therapy." The data provided in the letter regarding ear barotrauma are confusing bfcause we did not classify our barotrauma into Teed types 1 to 4. In our hyperbaric therapy patients, 79 sustained otalgia, two had tooth pain, two had sinus pain, one had epistaxis, and two patients sustained tympanic membrane rupture. We consider only the occurrence of epistaxis and tympanic rupture to represent actual barotrauma. Anatomic injury cannot be substantiated on the basis of pain alone. As such, our barotrauma complication rate was 1% (three of 297) and was similar to the 5% rate seen at MIEMSS. Whether prophylactic myringotomies are indicated is controversial. Some authors view their use as elective in comatose patients, particularly in the setting of severe carbon monoxide poisoning. ~ Both of our patients who sustained tympanic membrane rupture were comatose. These two complications would have been avoided had myringotomies been performed in all 66 of our comatose patients. We are, however, unaware of clinical studies indicating that outcome {specifically round window trauma and/or neurologic sequelae) in comatose patients is influenced by prophylactic myringotomy use. We, therefore, continue not to use this modality prior to hyperbaric therapy. We agree that dives should be modified when otalgia occurs, so as to avoid tympanic membrane rupture. Our hyperbaric facility will not proceed with the hyperbaric dive of an alert patient with ear pain unless it has been ameliorated by delayed descent, nasal neosynephrine (1%), and/ or oral pseudoephedrine (60 rag). If these methods fail, the dive can be aborted electively. In fact, five dives were terminated prematurely in our study "because of otalgia in the presence of complete clinical recovery." The issue of oxygen-related seizures is difficult to clar-

ify as there is no clinically accurate way to distinguish this type of seizure from one induced by carbon monoxide toxicity. At best, one could surmise that a new-onset seizure that occurs during hyperbaric therapy and resolves on the removal of the supplemental oxygen is secondary to oxygen toxicity, z Only one of the 14 hyperbaric chamber seizures in our series was believed to be oxygen-related. We considered describing this seizure as an oxygen-toxic seizure, but declined to do so because of an inability to exclude carbon monoxide as the etiology of the seizure. Classifying the one likely oxygen-related seizure as oxygen-toxic results in an incidence of 0.3% (one of 297), similar to the 0.5% rate seen at MIEMSS. The letter suggests that a reduction in oxygen-toxic seizures may occur if the duration of therapy is reduced to 46 minutes (two half-lives). We believe that the majority of our chamber seizures were carbon monoxide-induced, such that changes in therapy duration are not likely to have an effect on the rate of chamber seizures. To our knowledge, no prospective studies identify the duration of hyperbaric therapy that optimizes o u t c o m e and minimizes complications such as oxygen-toxic seizures. Incidentally, in the manuscript, carboxyhemoglobin (COHb] levels were listed as "rag-percent." The actual levels should be listed by "percent." We look forward to prospective research that clarifies the issues raised in our manuscript and their letter.

EP Sloan, MD DG Murphy, MD R Hart, MD M A Cooper, MD T Tumbull, MD RS Barreca, MD B E]lerson, RRT Trauma Unit Cook County Hospital Chicago 1. Kindwall EP, Goldmann RW: Complications of hyperbaric therapy, in Hyperbaric Medicine Procedures. Chicago, St Lukes Medical Center, 1988, p 135q41. 2. Myers RAM {ed): Hyperbaric Oxygen Therapy A Committee Report. Undersea and Hyperbaric Medical Society, Inc, 1986.

Additional Causes of Priapism To the Editor." We read with interest the review on priapism by O'Brien et al [September 1989;18:980-983]. The authors list the possible causes for priapism and state that "every effort must be made in the initial evaluation to identify by history one of the underlying causes previously mentioned above." While we agree with this statement, we think that the list of possible causes provided by the authors is incomplete and should include some other entities. Priapism was observed in 17 of 3,337 men and boys either during or several hours after dialysis. 1 In our experi178/1357

ence, priapism is a frequent manifestation of scorpion sting and occurred in 18 of 40 boys after being stung by scorpions {mostly the species Buthus quinquestriatus). ~ Other less frequent causes of priapism include amyloidosis 3 and black widow spider bites. 4

Yona Amitai, MD Samuel Heyman, MD Departments of Pediatrics and Emergency Medicine Hadassah University Hospital Mt Scopus, Jerusalem, Israel

Annals of Emergency Medicine

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Nephrol 1986;6:358-361.

1. Singhal PC, Lynn RI, Scharschrnidt LA: Priapism and dialysis. Am J

3. Lopan DI, Graham AR, Bangert JL, et al: Amyloidosis presenting as priapism. Urology 1980;15:167-170.

2. Amitai Y, Mines Y, Aker M, et al: Scorpion sting in children. A review of 51 cases. Clin Pediatr 1985;24:136-140.

4. stiles AD: Priapism following a black widow spider bite. Clin Pediatr 1982;21:174-175.

19:11 November 1990

Annals of Emergency Medicine


Additional causes of priapism.

CORRESPONDENCE incidence of complications in a group of carbon monoxide-intoxicated patients receiving hyperbaric oxygen therapy." We agree that such...
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