Correspondence UNTOWARD REACTION TO ADENOSINE THERAPY FOR SUPRAVENTRICULAR TACHYCARDIA
triphosphate theraDeutic
To the Editor:-1 found the presentation of cases and discussion of the clinical application of adenosine for supraventricular tachycardia by Reed et al to be timely and informative. However, I would like to bring to your attention a few errata and personal observations. The authors state that adenosine “. . . is completely inhibited by xanthine derivatives and therefore may be ineffective if the patient has ingested theophylline or caffeine.“’ Methylxanthines are competitive inhibitors of adenosine as they are both structurally nucleosides.‘z3 As such, in the presence of methylxanthines, larger doses of adenosine may be required or it may not be effective.4.s Anecdotally, having routinely obtained histories of methylxanthine ingestion, I have noted that conversion is not common after the initial 6-mg bolus in these patients. Many will, however, convert after the second or third 12-mg bolus. A significant percentage of patients with supraventricular tachycardia have consumed caffeine. Indeed, it may be a contributing factor. Competitive inhibition by the methylxanthines should not be considered a contraindication to adenosine use. There is no evidence to suggest an increased incidence of adverse reactions in this setting. Figures 2 and 4 in the report appear to have inaccurate electrocardiographic interpretations.’ After the period of asystole in Figure 2, the patient converts to a sinus bradycardia at 48 beats per minute rather than the captioned “irregular junctional rhythm.” Conversely, in Figure 4 the reentrant tachycardia resolves, leaving a junctional rhythm rather than “sinus bradycardia at a rate of 48 beats per minute” as captioned. The authors aptly conclude that the emergency physician should be prepared for the described untoward reactions to adenosine administration, especially when prolonged and associated with syncope and hypotension. In addition to external pacing availability, the team should be prepared to initiate resuscitative measures should asystole or heart block be prolonged. I have found in more than 30 applications of the drug one case of hypotension requiring prolonged emergency department treatment, but no admissions for adverse effects. Alternatively, the incidence of briefly symptomatic high-grade heart blocks of several seconds’ duration is quite frequent. 4*6I have found it useful to mentally prepare the patient, as well as the nursing staff, for this. After a few deep breaths, most patients find this experience well tolerated.
The authors reply:-We thank Dr Sobel for his erudite comments. We agree that adenosine is competitively rather than “completely” inhibited by methylxanthines and we should have selected our words more carefully. We did not, however, state that adverse reactions to adenosine are more common among patients who have ingested xanthine derivatives as Dr Sobel implies. Rather, we simply pointed out that the drug might be ineffective in these patients when given in the recommended doses. The manufacturer points this out in the packet insert, and this contention is reiterated in all of the articles listed in our bibliography, Dr Sobel’s anecdotal experience notwithstanding. In regard to Dr Sobel’s interpretation of the rhythm strips presented in the figures, we must disagree. Unfortunately, due to space limitations it is impossible to publish all of the various strips for each patient. Dr Sobel’s opinions are based on an incomplete data base. In Figure 2, patient no. 1 has a PR interval of 0.08 seconds. Prior to her current arrhythmic event and subsequently, when the patient was clearly in sinus rhythm, her PR interval measures 0.12 seconds. During the continuous monitoring of the patient following the end of the published tracing the P waves marched through the QRS and became inverted despite no change in QRS morphology. We adhere to the adage that “neither P wave polarity nor the PR interval are dependent guides to the origin of the atrial impulse.“’ Given all the data in this case we believe our interpretation of the rhythm as published is the most plausible. Patient no. 2 is in sinus bradycardia in Figure 4. While difficult to see in this lead II tracing, the P waves are present. On subsequent 12-lead tracings when sinus rhythm is clearly present P waves remain somewhat difficult to see in this lead. Interpretations of the specific rhythms are, in any case, peripheral to the important message of our report; namely, practitioners must be prepared to deal with the potential adverse consequences when administering adenosine.
1990;68:337-343
Safety, J Med
’
FCCM
The Department of Emergency Medicine Orlando Regional Medical Center Orlando, FL The Division of Emergency Medicine Department of Surgery University of Florida College of Medicine Gainsville, FL
South Seminole Community Hospital Longwood, FL
1. Reed R, Falk JL, O’Brien J: Untoward reaction to adenosine therapy for supraventricular tachycardia. Am J Emerg Med 1991;9:566-570 2. Clarke B, Coupe M: Cellular mechanisms, pathophysiological roles and clinical applications. Int J Cardiol 1989;23:1-10 3. DiMarco JP: Adenosine and supraventricular tachycardia. In Pelleg A, Michelson E, Dreifus LS (eds): Cardiac Electrophvsiology and Pharmacology of Adendsine and ATP: Basid and Clinical AsDects. New York. NY. Liss. 1987. DD 283-299 4. Cairns C, Niemann JT:‘lntr&endus adinbsine in the emergency department management of paroxysmal supraventricular tachycardia. Ann Emerg Med 1991;7:717-721 5. DiMarco JP, Sellers TD, Berne RM, et al: Adenosine: Electrophysiological effects and therapeutic use for terminating paroxysmal supraventricular tachycardia. Circulation 1983;68: 1254-l 263 6. Sharma AD, Klein QJ, Yee R: Intravenous adenosine
tachycardia: utility. Am
JAY L. FALK MD, FACEP, RHETT A. REED, MD JOHN F. O’BRIEN, MD
RICHARD M. SOBEL, MD
References
during wide QRS complex efficacv and diaanostic
References 1. Waldo AL, James TN: A retrospective rhythm. Circulation 1973;47:222-224
look
at A-V nodal
METAMUCIL BEZOAR: AN UNUSUAL CAUSE OF SMALL BOWEL OBSTRUCTION To the Editor:-Bezoars, tightly packed masses of fruit or vegetable matter, hair, or other material that forms in the gastrointestinal tract,’ are a recognized but uncommon cause of gastrointestinal tract obstruction. Medications implicated in bezoar formation include cholestyramine, aluminum hydroxide gel, polystyrene sodium sulfonate (Kayexalate, Winthrop Pharmaceuticals, New York, NY), vitamin C tablets, antacid tablets, iron tablets, Isocal (Mead Johnson, Evansville, IN), Serutan (Beecham Laboratories, Philadelphia, PA) (causing esophageal obstruction), and psyllium husks (causing a colonic bezoar).‘-5 Metamucil (psyllium hydrophilic mu393
394
AMERICAN JOURNAL OF EMERGENCY MEDICINE n Volume 10, Number 4 m July 1992
FIGURE 1. Photograph demonstrating the semi-solid mass that forms when Metamucil is prepared in the fashion described by the patient. cilloid, Proctor and Gamble, Cincinnati, OH) is a bulk laxative derived from the husk of the psyllium seed, Pfanrago ovatu. Presented is the first reported case of probable gastric outlet and proximal small bowel obstruction secondary to an improperly prepared dose of Metamucil. A 47-year-old previously healthy male presented to the emergency department with the complaint of 8 hours of colicky. epigastric abdominal pain. The pain, which was of sudden onset and radiated to his back, began approximately 30 minutes after his morning dose of Metamucil. Intermittent nausea and vomiting accompanied the pain. Several days prior to evaluation, the patient noticed his stools had decreased in caliber and were lighter in color than normal. The patient denied chest pain. shortness of breath, fevers, hematemesis, or melena. There was no prior history of biliary tract, pancreatic, or ulcer disease. Past abdominal surgical history was negative. The patient denied tobacco use and drank “one pitcher” of beer per week. His only medication was Metamucil, which he took daily to maintain bowel regularity. Initial physical examination revealed a well-nourished, welldeveloped male in obvious distress secondary to abdominal pain. Vital signs were a temperature of 97.2”F. pulse, 79 beats per minute; blood pressure, 148/100 mm Hg; and respiratory rate, 20 breaths per minute. The abdomen was mildly distended. had diminished bowel sounds throughout, and had percussive tympany over the epigastrium. There was epigastric and right upper quadrant tenderness to palpation with a positive Murphy’s sign. No masses were palpable and signs of peritoneal inflammation were absent. Genital examination was normal and rectal examination revealed a normal sized, nontender prostate and yellow, heme-negative stool. A complete blood-count revealed a hematocrit of 48.6% and a white blood count of 11,800 per mm3. Serum electrolyte panel results were sodium of 134 mEq/L; potassium, 4.0 mEq/L; chloride, 103 mEq/L; carbon dioxide. 22 mEq/L; blood urea nitrogen, 14 mg/ dL; creatinine, 1.1 mg/dL; and glucose, 143 mg/dL. Liver function tests were alkaline phosphatase, 119 U/L; aspartate aminotransferase, 36 U/L; alanine aminotransferase, 61 U/L; lactate dehydrogenase, 651 U/L; total bilirubin 0.8 mg/dL; and amylase, 47 U/L. Urinalysis was normal. Abdominal radiographs were initially interpreted as having nonspecific findings. Formal radiologic interpretation described an edematous loop of fluid-filled bowel, suggesting possible jejunal obstruction. While in the emergency department, the patient received 50 mg of ranitidine hydrochloride intravenously, and 20 mg of dicyclomine hydrochloride intramuscularly without relief. An 18-french nasogas-
tric tube was placed and low intermittent suctioning retrieved a small amount of gastric secretions and relieved the patient’s vomiting. The preliminary impression was biliary colic secondary to cholelithiasis. Ultrasound of the right upper quadrant failed to visualize the gallbladder. Hepatobiliary scan showed patent common and cystic ducts. During this study, morphine sulfate, 0.04 mg/kg. was given by slow intravenous infusion to enhance gallbladder visualization. This induced severe retching and vomiting which produced numerous. large, sticky masses of fibrous material. The gallbladder was visualized and in normal position. Two hours after vomiting the patient was asymptomatic. The patient was questioned further regarding dietary history. He denied excessive or unusual fruit or bran ingestion. Normally the patient mixed his daily dose (“one shot glass-full”) of Metamucil in a full glass of fruit juice. However. on the morning of admission, he had run out of fruit juice with which to mix his daily dose of Metamucil and had just enough juice to immerse the powder in the bottom of his glass. Being determined to take his medicine, the patient reported he had “chewed it down”. A double contrast upper gastrointestinal tract series performed I month after discharge was normal. The patient remained symptom free at last contact, 2 months after discharge. A comprehensive review by DeBakey and Ochsner6 classified
FIGURE 2. Photograph demonstrating the semi-solid mass that forms when Metamucil is prepared in the fashion described by the patient.
395
CORRESPONDENCE
bezoars into four varieties: trichobezoars (composed of hair), phytobezoars (composed of plant material), trichophytobezoars (composed of hair and plant material), and concretions (composed of medications or other substances that form a mass). Although the majority of bezoars form in patients with a prior history of gastroduodenal surgery or impaired gastrointestinal motility,’ small bowel obstruction due to phytobezoars in the normal gastrointestinal tract has been reported.’ Patients with bezoars may present with dyspepsia and epigastric discomfort, as well as symptoms and signs of gastrointestinal tract obstruction.’ The most common complications of bezoars are intestinal obstruction and gastroduodenal ulceration. Metamucil (psyllium hydrophilic mucilloid) is a bulk forming, therapeutic fiber for restoring and maintaining bowel regularity.8 The fiber source is the husk of the psyllium seed, Planrago ovata. Recommended dosage is one rounded teaspoonful in 8 ounces of liquid.8 This patient reported that he poured his usual dose, “one shot glass-full”, of Metamucil into a glass but did not have enough liquid to fully immerse the powder. Despite this apparent obstacle, the patient “chewed it down”. When the author prepared the Metamucil in the fashion described by the patient, a semi-solid mass formed (see Figures 1 and 2). Adverse reactions to Metamucil and other bulk laxatives are rare.’ The product label warns of an allergic reaction to inhaled or ingested psyllium. Severe adverse effects of bulk laxatives such as bowel and/or esophageal obstruction, swelling or blockage of the throat, choking, or asphyxiation have occurred when insufficient liquid has been administered with some bulk laxatives.’ When prepared with insufftcient liquid, a semi-solid mass forms rather than a viscous solution and may cause these more severe adverse effects.’ Serutan, a brand of psyllium hydrophilic mucilloid, prepared with insufftcient liquid has caused esophageal obstruction4.” Treatment of bezoars is dependent on their location in the gastrointestinal tract.’ Small bowel bezoars are often treated surgically while gastric bezoars have been successfully treated by endoscopic fragmentation and enzyme irrigation.’ In the present case, it is likely that gastric decompression and the patient’s vomiting relieved a probable gastric outlet and proximal small bowel obstruction caused by the semi-solid Metamucil. WILLIAMJ. FROHNA, MD Madigan Army Medical Center Tacoma,
WA
The opinions and assertions contained herein are the private views of the author and are not to be construed as official views of the United States Army or the Department of Defense.
References 1. Goldstein due to bezoars. 2. Korenman from medication
S. Lewis J, Rothstein R: intestinal obstruction Am J Gastroenterol 1984;79:313-318 M, Stubbs M, Fish J: Intestinal bezoars. JAMA 1978;240:54-55
obstruction
3. O’Malley J, Ferrucci J, Goodgame T: Medication bezoar: Intestinal obstruction by an Isocal@ bezoar. Gastrointest Radio1 1981;6:141-144 4. Hinkel L: Complete obstruction of the esophagus ing Serutan@ ingestion. JAMA 1951;146:1129-1131
follow-
5. Agha F, Nostrant T, Fiddian-Green R: “Giant colonic bezoar:” A medication bezoar due to psyllium seed husks. Am J Gastroenterol 1984;79:319-321 6. DeBakey M, Ochsner A: Bezoars and concretions, a comprehensive review of the literature with an analysis of 303 collected cases and a presentation of 8 additional cases. Surgery 1939;5:132-160 7. Swift R, Wood C, Hershman M: Small bowel obstruction due to phytobezoars in the intact gastrointestinal tract. J R Coil Surg Edinb 1989;34:267-269
8. Metamucil. ell, NJ, Medical
In Physicians’ Economics
Desk Reference (ed 45). OradData, 1991, pp 1740-1741
9. Bulk laxatives. In American Hospital Formulary Drug Information 91. Bethesda, MD, American Society pital Pharmacists, 1991, p 1721 10. Melamed A, Marck A: Esophageal rutan@. JAMA 1953;152:318-319
obstruction
Service of Hos-
due to Se-
GLYCOPYRROLATE FOR ASTHMA To the Editor:-Since the publication of our recent article,’ we are now recommending a minimum 1-mg dose of nebulized glycopyrrolate (versus the 0.6 mg dose traditionally used in our medical center and cited in Tables 1 and 2 of our article). Although the optimal dose of glycopyrrolate aerosol for the emergency department (ED) treatment of asthma is yet to be established, we recommend the minimum I-mg dose based on the following factors. First, in a study of stable asthmatics, a dose of as little as 0.1 mg given via an experimental metered dose inhaler was as effective as 1.2 mg.2 Doses of aerosol medications given via nebulizers are usually at least 10 times the doses given via metered dose inhalers. Thus, our recommendation of at least a I-mg dose. The second pertinent factor is that a study which we cited in our article’ found that 2 mg nebulized glycopyrrolate was very effective as a single agent in the treatment of acute asthma.’ Unfortunately, glycopyrrolate is currently available only as an intravenous solution at a concentration of 0.2 mg/mL with the resulting volume of IO mL (2 mg) close to being excessive for the nebulizer cup. We routinely mix a beta agonist such as albuterol with glycopyrrolate at the time of administration, so that 10 mL plus 3 mL (albuterol plus saline) would clearly be excessive volume. On the other hand, 1 mg glycopyrrolate is a 5-mL volume, and therefore, acceptable with the addition of the 3 mL volume of albuterol and saline. Until further research establishes the optimal dose of glycopyrrolate in the ED treatment of asthma, a I-mg dose mixed with a beta agonist would seem appropriate. Alternatively, a beta agonist could be given first, immediately followed by 2 mg glycopyrrolate with subsequent continued intensive inhaled beta agonist therapy. Although combined use of glycopyrrolate and beta agonist in the ED has not been proven effective, use of ipratropium nebulized solution with the inihl dose of beta agonist in the ED is proven4*’ Until ipratropium nebulizer solution is available in the United States, clinicians have the choice of using either nebulized glycopyrrolate or ipratropium metered dose inhaler plus spacer device in the ED with the initial dose of beta agonist. Another question pertinent to ED asthma therapy has been raised since our article was written. In a very recent study by Wrenn et aL6 aminophylline therapy in the ED was reported to reduce hospitalizations (versus a placebo group, with both groups receiving inhaled beta agonists and systemic glucocorticoids). The authors could not explain these findings, and aminophylline provided no benefit in terms of pulmonary function or subjective patient response. These authors correctly emphasized that further study is clearly required before this agent can be recommended for routine in the ED therapy of asthma. With a much larger patient population than Wrenn et al,6 we have found no benetit of aminophyhine in reducing hospital admission rates. Combining patients in our recent article with patients from another study of ours,’ we noted that 9.1% of 342 adult asthmatics were admitted to the hospital. Although none of these patients received any theophylline product in our ED, this hospital admission rate is comparable to the rate reported for the aminophylline group in the paper by Wrenn et al (6%) and is much lower than the admission rate in their placebo group (1%). Since our hospitalization criteria are very similar to those described by Wrenn et al, the reasons for this difference cannot be readily determined. The mean length of stay in the ED for our patients was 4.4 hours. Considering the risk of serious toxicity with this agent and its ques-
triphosphate theraDeutic
To the Editor:-1 found the presentation of cases and discussion of the clinical application of adenosine for supraventricular tachycardia by Reed et al to be timely and informative. However, I would like to bring to your attention a few errata and personal observations. The authors state that adenosine “. . . is completely inhibited by xanthine derivatives and therefore may be ineffective if the patient has ingested theophylline or caffeine.“’ Methylxanthines are competitive inhibitors of adenosine as they are both structurally nucleosides.‘z3 As such, in the presence of methylxanthines, larger doses of adenosine may be required or it may not be effective.4.s Anecdotally, having routinely obtained histories of methylxanthine ingestion, I have noted that conversion is not common after the initial 6-mg bolus in these patients. Many will, however, convert after the second or third 12-mg bolus. A significant percentage of patients with supraventricular tachycardia have consumed caffeine. Indeed, it may be a contributing factor. Competitive inhibition by the methylxanthines should not be considered a contraindication to adenosine use. There is no evidence to suggest an increased incidence of adverse reactions in this setting. Figures 2 and 4 in the report appear to have inaccurate electrocardiographic interpretations.’ After the period of asystole in Figure 2, the patient converts to a sinus bradycardia at 48 beats per minute rather than the captioned “irregular junctional rhythm.” Conversely, in Figure 4 the reentrant tachycardia resolves, leaving a junctional rhythm rather than “sinus bradycardia at a rate of 48 beats per minute” as captioned. The authors aptly conclude that the emergency physician should be prepared for the described untoward reactions to adenosine administration, especially when prolonged and associated with syncope and hypotension. In addition to external pacing availability, the team should be prepared to initiate resuscitative measures should asystole or heart block be prolonged. I have found in more than 30 applications of the drug one case of hypotension requiring prolonged emergency department treatment, but no admissions for adverse effects. Alternatively, the incidence of briefly symptomatic high-grade heart blocks of several seconds’ duration is quite frequent. 4*6I have found it useful to mentally prepare the patient, as well as the nursing staff, for this. After a few deep breaths, most patients find this experience well tolerated.
The authors reply:-We thank Dr Sobel for his erudite comments. We agree that adenosine is competitively rather than “completely” inhibited by methylxanthines and we should have selected our words more carefully. We did not, however, state that adverse reactions to adenosine are more common among patients who have ingested xanthine derivatives as Dr Sobel implies. Rather, we simply pointed out that the drug might be ineffective in these patients when given in the recommended doses. The manufacturer points this out in the packet insert, and this contention is reiterated in all of the articles listed in our bibliography, Dr Sobel’s anecdotal experience notwithstanding. In regard to Dr Sobel’s interpretation of the rhythm strips presented in the figures, we must disagree. Unfortunately, due to space limitations it is impossible to publish all of the various strips for each patient. Dr Sobel’s opinions are based on an incomplete data base. In Figure 2, patient no. 1 has a PR interval of 0.08 seconds. Prior to her current arrhythmic event and subsequently, when the patient was clearly in sinus rhythm, her PR interval measures 0.12 seconds. During the continuous monitoring of the patient following the end of the published tracing the P waves marched through the QRS and became inverted despite no change in QRS morphology. We adhere to the adage that “neither P wave polarity nor the PR interval are dependent guides to the origin of the atrial impulse.“’ Given all the data in this case we believe our interpretation of the rhythm as published is the most plausible. Patient no. 2 is in sinus bradycardia in Figure 4. While difficult to see in this lead II tracing, the P waves are present. On subsequent 12-lead tracings when sinus rhythm is clearly present P waves remain somewhat difficult to see in this lead. Interpretations of the specific rhythms are, in any case, peripheral to the important message of our report; namely, practitioners must be prepared to deal with the potential adverse consequences when administering adenosine.
1990;68:337-343
Safety, J Med
’
FCCM
The Department of Emergency Medicine Orlando Regional Medical Center Orlando, FL The Division of Emergency Medicine Department of Surgery University of Florida College of Medicine Gainsville, FL
South Seminole Community Hospital Longwood, FL
1. Reed R, Falk JL, O’Brien J: Untoward reaction to adenosine therapy for supraventricular tachycardia. Am J Emerg Med 1991;9:566-570 2. Clarke B, Coupe M: Cellular mechanisms, pathophysiological roles and clinical applications. Int J Cardiol 1989;23:1-10 3. DiMarco JP: Adenosine and supraventricular tachycardia. In Pelleg A, Michelson E, Dreifus LS (eds): Cardiac Electrophvsiology and Pharmacology of Adendsine and ATP: Basid and Clinical AsDects. New York. NY. Liss. 1987. DD 283-299 4. Cairns C, Niemann JT:‘lntr&endus adinbsine in the emergency department management of paroxysmal supraventricular tachycardia. Ann Emerg Med 1991;7:717-721 5. DiMarco JP, Sellers TD, Berne RM, et al: Adenosine: Electrophysiological effects and therapeutic use for terminating paroxysmal supraventricular tachycardia. Circulation 1983;68: 1254-l 263 6. Sharma AD, Klein QJ, Yee R: Intravenous adenosine
tachycardia: utility. Am
JAY L. FALK MD, FACEP, RHETT A. REED, MD JOHN F. O’BRIEN, MD
RICHARD M. SOBEL, MD
References
during wide QRS complex efficacv and diaanostic
References 1. Waldo AL, James TN: A retrospective rhythm. Circulation 1973;47:222-224
look
at A-V nodal
METAMUCIL BEZOAR: AN UNUSUAL CAUSE OF SMALL BOWEL OBSTRUCTION To the Editor:-Bezoars, tightly packed masses of fruit or vegetable matter, hair, or other material that forms in the gastrointestinal tract,’ are a recognized but uncommon cause of gastrointestinal tract obstruction. Medications implicated in bezoar formation include cholestyramine, aluminum hydroxide gel, polystyrene sodium sulfonate (Kayexalate, Winthrop Pharmaceuticals, New York, NY), vitamin C tablets, antacid tablets, iron tablets, Isocal (Mead Johnson, Evansville, IN), Serutan (Beecham Laboratories, Philadelphia, PA) (causing esophageal obstruction), and psyllium husks (causing a colonic bezoar).‘-5 Metamucil (psyllium hydrophilic mu393
394
AMERICAN JOURNAL OF EMERGENCY MEDICINE n Volume 10, Number 4 m July 1992
FIGURE 1. Photograph demonstrating the semi-solid mass that forms when Metamucil is prepared in the fashion described by the patient. cilloid, Proctor and Gamble, Cincinnati, OH) is a bulk laxative derived from the husk of the psyllium seed, Pfanrago ovatu. Presented is the first reported case of probable gastric outlet and proximal small bowel obstruction secondary to an improperly prepared dose of Metamucil. A 47-year-old previously healthy male presented to the emergency department with the complaint of 8 hours of colicky. epigastric abdominal pain. The pain, which was of sudden onset and radiated to his back, began approximately 30 minutes after his morning dose of Metamucil. Intermittent nausea and vomiting accompanied the pain. Several days prior to evaluation, the patient noticed his stools had decreased in caliber and were lighter in color than normal. The patient denied chest pain. shortness of breath, fevers, hematemesis, or melena. There was no prior history of biliary tract, pancreatic, or ulcer disease. Past abdominal surgical history was negative. The patient denied tobacco use and drank “one pitcher” of beer per week. His only medication was Metamucil, which he took daily to maintain bowel regularity. Initial physical examination revealed a well-nourished, welldeveloped male in obvious distress secondary to abdominal pain. Vital signs were a temperature of 97.2”F. pulse, 79 beats per minute; blood pressure, 148/100 mm Hg; and respiratory rate, 20 breaths per minute. The abdomen was mildly distended. had diminished bowel sounds throughout, and had percussive tympany over the epigastrium. There was epigastric and right upper quadrant tenderness to palpation with a positive Murphy’s sign. No masses were palpable and signs of peritoneal inflammation were absent. Genital examination was normal and rectal examination revealed a normal sized, nontender prostate and yellow, heme-negative stool. A complete blood-count revealed a hematocrit of 48.6% and a white blood count of 11,800 per mm3. Serum electrolyte panel results were sodium of 134 mEq/L; potassium, 4.0 mEq/L; chloride, 103 mEq/L; carbon dioxide. 22 mEq/L; blood urea nitrogen, 14 mg/ dL; creatinine, 1.1 mg/dL; and glucose, 143 mg/dL. Liver function tests were alkaline phosphatase, 119 U/L; aspartate aminotransferase, 36 U/L; alanine aminotransferase, 61 U/L; lactate dehydrogenase, 651 U/L; total bilirubin 0.8 mg/dL; and amylase, 47 U/L. Urinalysis was normal. Abdominal radiographs were initially interpreted as having nonspecific findings. Formal radiologic interpretation described an edematous loop of fluid-filled bowel, suggesting possible jejunal obstruction. While in the emergency department, the patient received 50 mg of ranitidine hydrochloride intravenously, and 20 mg of dicyclomine hydrochloride intramuscularly without relief. An 18-french nasogas-
tric tube was placed and low intermittent suctioning retrieved a small amount of gastric secretions and relieved the patient’s vomiting. The preliminary impression was biliary colic secondary to cholelithiasis. Ultrasound of the right upper quadrant failed to visualize the gallbladder. Hepatobiliary scan showed patent common and cystic ducts. During this study, morphine sulfate, 0.04 mg/kg. was given by slow intravenous infusion to enhance gallbladder visualization. This induced severe retching and vomiting which produced numerous. large, sticky masses of fibrous material. The gallbladder was visualized and in normal position. Two hours after vomiting the patient was asymptomatic. The patient was questioned further regarding dietary history. He denied excessive or unusual fruit or bran ingestion. Normally the patient mixed his daily dose (“one shot glass-full”) of Metamucil in a full glass of fruit juice. However. on the morning of admission, he had run out of fruit juice with which to mix his daily dose of Metamucil and had just enough juice to immerse the powder in the bottom of his glass. Being determined to take his medicine, the patient reported he had “chewed it down”. A double contrast upper gastrointestinal tract series performed I month after discharge was normal. The patient remained symptom free at last contact, 2 months after discharge. A comprehensive review by DeBakey and Ochsner6 classified
FIGURE 2. Photograph demonstrating the semi-solid mass that forms when Metamucil is prepared in the fashion described by the patient.
395
CORRESPONDENCE
bezoars into four varieties: trichobezoars (composed of hair), phytobezoars (composed of plant material), trichophytobezoars (composed of hair and plant material), and concretions (composed of medications or other substances that form a mass). Although the majority of bezoars form in patients with a prior history of gastroduodenal surgery or impaired gastrointestinal motility,’ small bowel obstruction due to phytobezoars in the normal gastrointestinal tract has been reported.’ Patients with bezoars may present with dyspepsia and epigastric discomfort, as well as symptoms and signs of gastrointestinal tract obstruction.’ The most common complications of bezoars are intestinal obstruction and gastroduodenal ulceration. Metamucil (psyllium hydrophilic mucilloid) is a bulk forming, therapeutic fiber for restoring and maintaining bowel regularity.8 The fiber source is the husk of the psyllium seed, Planrago ovata. Recommended dosage is one rounded teaspoonful in 8 ounces of liquid.8 This patient reported that he poured his usual dose, “one shot glass-full”, of Metamucil into a glass but did not have enough liquid to fully immerse the powder. Despite this apparent obstacle, the patient “chewed it down”. When the author prepared the Metamucil in the fashion described by the patient, a semi-solid mass formed (see Figures 1 and 2). Adverse reactions to Metamucil and other bulk laxatives are rare.’ The product label warns of an allergic reaction to inhaled or ingested psyllium. Severe adverse effects of bulk laxatives such as bowel and/or esophageal obstruction, swelling or blockage of the throat, choking, or asphyxiation have occurred when insufficient liquid has been administered with some bulk laxatives.’ When prepared with insufftcient liquid, a semi-solid mass forms rather than a viscous solution and may cause these more severe adverse effects.’ Serutan, a brand of psyllium hydrophilic mucilloid, prepared with insufftcient liquid has caused esophageal obstruction4.” Treatment of bezoars is dependent on their location in the gastrointestinal tract.’ Small bowel bezoars are often treated surgically while gastric bezoars have been successfully treated by endoscopic fragmentation and enzyme irrigation.’ In the present case, it is likely that gastric decompression and the patient’s vomiting relieved a probable gastric outlet and proximal small bowel obstruction caused by the semi-solid Metamucil. WILLIAMJ. FROHNA, MD Madigan Army Medical Center Tacoma,
WA
The opinions and assertions contained herein are the private views of the author and are not to be construed as official views of the United States Army or the Department of Defense.
References 1. Goldstein due to bezoars. 2. Korenman from medication
S. Lewis J, Rothstein R: intestinal obstruction Am J Gastroenterol 1984;79:313-318 M, Stubbs M, Fish J: Intestinal bezoars. JAMA 1978;240:54-55
obstruction
3. O’Malley J, Ferrucci J, Goodgame T: Medication bezoar: Intestinal obstruction by an Isocal@ bezoar. Gastrointest Radio1 1981;6:141-144 4. Hinkel L: Complete obstruction of the esophagus ing Serutan@ ingestion. JAMA 1951;146:1129-1131
follow-
5. Agha F, Nostrant T, Fiddian-Green R: “Giant colonic bezoar:” A medication bezoar due to psyllium seed husks. Am J Gastroenterol 1984;79:319-321 6. DeBakey M, Ochsner A: Bezoars and concretions, a comprehensive review of the literature with an analysis of 303 collected cases and a presentation of 8 additional cases. Surgery 1939;5:132-160 7. Swift R, Wood C, Hershman M: Small bowel obstruction due to phytobezoars in the intact gastrointestinal tract. J R Coil Surg Edinb 1989;34:267-269
8. Metamucil. ell, NJ, Medical
In Physicians’ Economics
Desk Reference (ed 45). OradData, 1991, pp 1740-1741
9. Bulk laxatives. In American Hospital Formulary Drug Information 91. Bethesda, MD, American Society pital Pharmacists, 1991, p 1721 10. Melamed A, Marck A: Esophageal rutan@. JAMA 1953;152:318-319
obstruction
Service of Hos-
due to Se-
GLYCOPYRROLATE FOR ASTHMA To the Editor:-Since the publication of our recent article,’ we are now recommending a minimum 1-mg dose of nebulized glycopyrrolate (versus the 0.6 mg dose traditionally used in our medical center and cited in Tables 1 and 2 of our article). Although the optimal dose of glycopyrrolate aerosol for the emergency department (ED) treatment of asthma is yet to be established, we recommend the minimum I-mg dose based on the following factors. First, in a study of stable asthmatics, a dose of as little as 0.1 mg given via an experimental metered dose inhaler was as effective as 1.2 mg.2 Doses of aerosol medications given via nebulizers are usually at least 10 times the doses given via metered dose inhalers. Thus, our recommendation of at least a I-mg dose. The second pertinent factor is that a study which we cited in our article’ found that 2 mg nebulized glycopyrrolate was very effective as a single agent in the treatment of acute asthma.’ Unfortunately, glycopyrrolate is currently available only as an intravenous solution at a concentration of 0.2 mg/mL with the resulting volume of IO mL (2 mg) close to being excessive for the nebulizer cup. We routinely mix a beta agonist such as albuterol with glycopyrrolate at the time of administration, so that 10 mL plus 3 mL (albuterol plus saline) would clearly be excessive volume. On the other hand, 1 mg glycopyrrolate is a 5-mL volume, and therefore, acceptable with the addition of the 3 mL volume of albuterol and saline. Until further research establishes the optimal dose of glycopyrrolate in the ED treatment of asthma, a I-mg dose mixed with a beta agonist would seem appropriate. Alternatively, a beta agonist could be given first, immediately followed by 2 mg glycopyrrolate with subsequent continued intensive inhaled beta agonist therapy. Although combined use of glycopyrrolate and beta agonist in the ED has not been proven effective, use of ipratropium nebulized solution with the inihl dose of beta agonist in the ED is proven4*’ Until ipratropium nebulizer solution is available in the United States, clinicians have the choice of using either nebulized glycopyrrolate or ipratropium metered dose inhaler plus spacer device in the ED with the initial dose of beta agonist. Another question pertinent to ED asthma therapy has been raised since our article was written. In a very recent study by Wrenn et aL6 aminophylline therapy in the ED was reported to reduce hospitalizations (versus a placebo group, with both groups receiving inhaled beta agonists and systemic glucocorticoids). The authors could not explain these findings, and aminophylline provided no benefit in terms of pulmonary function or subjective patient response. These authors correctly emphasized that further study is clearly required before this agent can be recommended for routine in the ED therapy of asthma. With a much larger patient population than Wrenn et al,6 we have found no benetit of aminophyhine in reducing hospital admission rates. Combining patients in our recent article with patients from another study of ours,’ we noted that 9.1% of 342 adult asthmatics were admitted to the hospital. Although none of these patients received any theophylline product in our ED, this hospital admission rate is comparable to the rate reported for the aminophylline group in the paper by Wrenn et al (6%) and is much lower than the admission rate in their placebo group (1%). Since our hospitalization criteria are very similar to those described by Wrenn et al, the reasons for this difference cannot be readily determined. The mean length of stay in the ED for our patients was 4.4 hours. Considering the risk of serious toxicity with this agent and its ques-
