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Pulsatile tinnitus during a valsalva maneuver in a patient with Wolff-Parkinson-White syndrome
Correspondence OBTUNDATION IN THE ELDERLY PATIENT To the Editor:-1 have concerns about the article by James Svenson entitled “Obtundation in the Elderly Patient: Presentation of a Drug Overdose,” in the November 1987 issue of AJEM. This 88-year-old woman presented because of obtundation and had clear mental status changes. With the exception of some drooling from the left side of the mouth, there was no evidence of any focal neurological abnormality. A diagnosis of cardiovascular accident was rendered. The following day a suicide note was found and a benzodiazepine overdose was diagnosed. The diagnosis of “cardiovascular event” is so nonspecific it is virtually meaningless. Even if one had meant to say “cerebrovascular accident,” one would be hardpressed to define the area within the brain that had been focally effected by a thrombotic event resulting only in mental status changes. For obtundation to occur, either the brainstem must be involved or bilateral involvement of the cerebral hemispheres must occur. There was no evidence of either of these in this patient’s presentation. NEAL LITTLE, MD Ann Arbor, Michigan
Reference 1. Svenson J: Obtundation in the elderly patient: Presentation of a drug overdose. Am J Emerg Med 1987;5:524-528
The author replies:-The admitting diagnosis of the patient in my article was “cerebrovascular accident,” rather than “cardiovascular accident,” and I apologize for not correcting the error during proofreading. I agree with Dr Little that one is hard pressed to fully explain this patient’s symptoms on the basis of a cerebrovascular accident. Certainly brainstem infarctions can lead to alterations in consciousness, but these are usually overshadowed by other, more dramatic, neurological signs. Perhaps the admitting diagnosis should have been “lethargy-? etiology.” Although the choice of admitting diagnosis by her attending physician may be questionable, neither I nor the journal have any control over the facts. I would emphasize that one of the major points of my article is to consider other diagnoses (for example, occult drug ingestion) in the elderly when the clinical data do not quite fit into some well-defined syndrome. I thank Dr Little for his comments. JAMESSVENSON,MD Madison, Wisconsin
The American Journal of Emergency Medicine invites correspondence, commentary, and criticism in the form of letters to the editor. Please address correspondence to The Editor: The American Journal of Emergency Medicine, 3800 Reservoir Rd, NW, Washington, DC 20007.
PULSATILE TINNITUS DURING A VALSALVA MANEUVER IN A PATIENT WITH WOLFF-PARKINSON-WHITE SYNDROME To the Editor:-Wolff-Parkinson-White (WPW) syndrome, a common cause of paroxysmal supraventricular tachycardia, was first described in 1930.’ Patients with this disease may have no complaints or may complain of palpitations, dyspnea, or chest pain. In those who are symptomatic, many have learned to end their discomfort by self-converting the tachycardia back into a normal sinus rhythm through the use of carotid massage or the Valsalva maneuver. Although the use of the Valsalva maneuver has frequently been recorded to be of benefit in these patients, the literature reveals no reports of pulsatile tinnitus occurring during the maneuver. We recently treated a patient with WPW syndrome whose conversion from a supraventricular tachycardia to a normal sinus rhythm was manifested by pulsatile tinnitus during his use of the Valsalva maneuver. A 63-year-old Hispanic man presented to the emergency department (ED) with a chief complaint of chest pain. The pain had begun earlier that day, was not associated with activity, and radiated into the left neck and arm. The pain lasted for approximately two hours, but was not present at the time of examination by the medical student. He reported having similar episodes of chest pain once every 3 to 4 months over the past 7 years. He noted that he could make the chest pain go away by taking rapid, forceful deep breaths, but when he did so he heard a rhythmic “clicking” in his ears. The pain would cease immediately after this measure. He denied any other cardiac or pulmonary symptomatology; his history was negative for palpitations, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, or dyspnea on exertion. His past history was remarkable only for a left ankle fracture and a stab wound to the abdomen. He took no medications at home and had no known allergies. Family history was unremarkable, but he acknowledged a one pack per day smoking history and an alcohol intake of many cans of beer per day, both of an unknown duration. On examination, he was a slightly obese, ill-kempt man who was alert, cooperative, and in no acute distress. The odor of alcohol was present on his breath. Initial vital signs showed a pulse of 88, respiratory rate 20, BP 124/70, and temperature of 95S”F. Examination of the head, ears, eyes, nose, and throat was unremarkable. The neck was supple with no adenopathy, jugular venous distension, or carotid bruits noted. Carotid upstroke was good bilaterally. The chest was clear to auscultation. Cardiovascular examination revealed a regular rate and rhythm with no murmur, S3, or S4 noted. Abdominal examination was benign. The extremities were without cyanosis or edema, and pulses were good throughout. The neurological examination was grossly intact. The diagnosis of unstable angina, rule out myocardial infarction, was entertained in light of the patient’s history of
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
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6, Number
chest pain. An intravenous (IV) line was established and oxygen was administered by nasal cannula. Initial laboratory values showed a WBC count of 7,500 with 39 polycites, 54 lymphocytes, 5 monocytes, 1 eosinophil, and 1 basophil; hemoglobin was 15.0 g/dL, hematocrit 44%, platelets 376,000, and RBC indices (mean corpuscular volume, mean corpuscular hemaglobin, and mean corpuscular hemaglobin concentration) were within normal limits. Chemistry revealed: sodium, 141; potassium, 3.3; chloride, 108; CO,, 21; BUN, 5; creatinine, 0.9; and glucose, 125. Creatinine phosphokinase was 148, lactate dehydrogenase was 147, and SGOT was 34. Room air arterial blood gases showed a pH of 7.39, p0, of 72 mmHg, and pC0, of 38 mmHg. Hemoglobin saturation was 95%. The ECG showed a normal sinus rhythm at a rate of 100 with left axis deviation. No evidence of ischemia, infarction, or conduction abnormality was noted. The medicine service was notified of a consultation for admission to rule out myocardial infarction. The patient was resting comfortably in the treatment area, his cardiac rhythm being monitored by telemetry. A few minutes later, the ED attending physician noted that the patient had initiated a supraventricular tachycardia with a rate near 150 beats per minute. The physician again evaluated the patient, who had now developed the sudden onset of chest pain. Vital signs revealed a pulse increase to 160 beats per minute, and systolic BP had fallen to 80 mmHg. The patient was placed in the Trendelenberg position and the BP increased to 90 mmHg systolic, without a change in pulse rate. The patient was asked to reproduce what he usually did at home to make the pain stop. The patient performed several repetitions of forceful inspiration and exhalation, which were recognized by the attending physician as a Valsalva maneuver. However, the pain continued and 2.5 mg IV verapamil were administered. The patient was asked to repeat the Valsalva maneuver. This time he reported hearing a rhythmic “clicking” sound in both ears, and as he did so the pain abruptly ceased. A review of the monitor strip taken during this episode demonstrated clearly the conversion of the patient’s tachycardia to a normal sinus rhythm (Fig 1). The patient was admitted to the medicine service with a diagnosis of supraventricular tachycardia. Myocardial infarction was ruled out through serial ECGs and cardiac en-
FIGURE 1. maneuver.
Monitor strip revealing conversion of a supraventricular
6 n November
1988
zyme determinations. Cardiology consultation was obtained, and it was felt that the patient had a WPW preexcitation syndrome using an accessory conduction pathway on the left side of the heart. It was noted that the findings suggestive of WPW syndrome were rate-dependent and seen only on ECGs performed at slower heart rates. These findings were not evident on the initial tracing done in the ED. Twentyfour-hour Holter monitoring confirmed the presence of delta waves at slower heart rates, and a three-minute run of SVT, thought to involve the left atrioventricular bypass tract in a retrograde fashion, was recorded. The patient did well throughout his hospital stay and was discharged to home on Inderal LA, 80 mg each morning. He was noted to be doing well on subsequent visits to the outpatient internal medicine clinic. In the case of this patient, the use of the Valsalva maneuver had been self-taught as a means of ending each episode of tachycardia (manifested clinically by chest pain). Of interest is the association between the use of this maneuver and the repetitive clicking sound he heard in his ears, a perception that might best be considered as pulsatile tinnitus. Although pulsatile tinnitus has been well described in the otologic literature,2.3 it has received scant notice elsewhere, and in no instance before has it been associated with the use of the Valsalva maneuver. Pulsatile tinnitus has been described as the hearing of rhythmic sounds that are synchronous with the pulse. The causes of pulsatile tinnitus may be divided into two groups. Those due to lesions of the arterial system of the head and neck include arteriovenous malformations, arterioarterial anastomoses, and intraluminal irregularities of the carotids (such as arteriosclerosis and fibromuscular dysplasia). Causes of pulsatile tinnitus of nonarterial origin include cervical venous hums, cardiac murmurs, abnormalities of the jugular bulb, increased intracranial pressure, and neoplasms of the middle ear and temporal bone.2 The management of pulsatile tinnitus in the ED includes a careful history, especially for the presence of decreased hearing, headache, or other neurological symptoms, and a meticulous physical examination to include auscultation of the carotids and auricular region. cardiovascular examination, ophthalmoscopy, and tympanoscopy. Referral to an otolaryngologist is essential. Further workup may include audiologic assessment,
tachycardia to a normal sinus rhythm during performance
of the Valsalva
CORRESPONDENCE
computed
tomography
of the head, and carotid or cerebral
angiography . HOWARD RODENBERG,MD MATTHEW GRATTON, MD
Truman Medical Center Kansas City, Missouri
References Wolff L, Parkinson J, White PD: Bundle branch block with short R-P interval in healthy young people prone to paroxysmal tachycardia. Am Heart J 1930;5:665 Levine SB, Snow JB Jr: Pulsatile tinnitus. Laryngoscope 1967;97:401-406 Sila CA, Furlan AJ, Little JR: Pulsatile tinnitus. Stroke 1987;18:252-256
POVIDONE-IODINE SOLUTIONS IN TRAUMATIC WOUND PREPARATION To the Editor:-AJEM published a letter by Michael S. Oberg, MD entitled “Povidone-Iodine Solutions in Traumatic Wound Preparation,“’ which contained opinions based on a very limited number of references. In addition, some of the references quoted have little or no relevance to the practical and proper use of povidone-iodine. Dr Oberg declares the data to be conflicting, yet reaches conclusions and a recommendation. The reason for conflicting data derives from the difficulties encountered in the studies reported rather than the failure of the agent. Numerous studies which are not cited conclusively demonstrate the usefulness of povidone-iodine solution in the management of wounds.‘-” KENNETH G. ROTHWELL, MD
Easton, Connecticut
References 1. Oberg MS: Povidone-iodine solutions in traumatic wound preparation. Am J Emerg Med 1987;5:553-555 (letter) 2. Garnes AL, Davidson E, Taylor LE, et al: Clinical evaluation of povidone-iodine spray in surgical practice. Am J Surg 1959;97:49-53 3. Lee BY, Trainor FS, Thoden WR: Topical application of povidone-iodine in the management of decubitis and stasis ulcers. J Am Geriatr Sot 1979;27:302-306 4. Kwaan JHM, Connolly JE: Successful management of prosthetic graft infection with continuous povidone-iodine irrigation. Arch Surg 1981;116:716-720 5. Morgan WJ: The effect of povidone-iodine aerosol spray on superficial wounds. Br J Clin Pratt 1979;33:109-110 6. Gilgore A: The use of povidone-iodine in the treatment of infected cutaneous ulcers. Curr Ther Res 1978;24:843-848 7. Stefanides MM, Copeland DE, Kominos SD, et al: In vitro penetration of topical antiseptics through eschar of burn patients. Ann Surg 1976;183:358-364 8. Wynn-Williams D, Monballiu G: The effects of povidoneiodine in the treatment of burns and traumatic losses of skin. Br J Plast Surg 1965;18:146-150 9. Connell JF Jr, Rousselet LM: Povidone-iodine: Extensive surgical evaluation of a new antiseptic agent. Am J Surg 1964;108:849-855 10. Linkner LM, Cloud DT, Trump DS, et al: Prevention of bac-
terial growth and local infection in burn wounds. J Ped Surg 1972;7:310-314 11. Georgide NG, Matton GE, Kessel FV: Facial burns. Plast Reconstr Surg 1962;29:648-657
The author replies:-1 have read Dr Rothwell’s letter and it is not clear to me that he read either the title or the body of my correspondence. Nor is it clear to me what his interest in the subject is. My interest is as an emergency physician who had to deal with one of those mundane but important issues that face us all in the emergency department (ED). My letter dealt with the use of povidone-iodine solutions on acute traumatic wounds in the ED, ie, lacerations. I offered it in the hope that other emergency physicians who have to deal with this issue might find it helpful. I fail to see that the references Dr Rothwell offers on the treatment of decubitus ulcers, stasis ulcers, cutaneous ulcers, penetration through bum eschar, and chronic bum care have much relevance to treatment of acute lacerations. Many of the references he cites were unearthed in my search but not used for the reasons noted or because some had been superseded by more recent studies. Elsewhere in the letter, I stated that povidoneiodine is a valuable agent (our own hospital uses it by the gallon); I just question its value in this context. I feel that my letter fairly summarized the recent and still somewhat sparse literature on this subject. The results are indeed conflicting and the conclusions I reached are clearly labeled as my own beliefs. I stand by the letter as written. Thank you for this opportunity to reply. MICHAEL S. OBERG, MD
Arlington, Texas
CHEMICAL STABILITY OF SUBLINGUAL NITROGLYCERIN TABLETS CARRIED ON PARAMEDIC VEHICLES To the Editor:-Sublingual nitroglycerin (NTG) has long been used for the treatment of patients with cardiac chest pain. Although its predominant action is as a venodilator effectively reducing cardiac preload, NTG also relaxes peripheral vascular smooth muscle, producing a fall in cardiac afterload as well.’ Both atherosclerotic and normal coronary arteries dilate following NTG administration.’ These vascular effects are the rationale for the administration of sublingual NTG tablets in patients experiencing angina pectoris, myocardial infarction, and acute pulmonary edema during the prehospital phase of illness. Upon exposure to air, NTG tablets begin to degrade, and their pharmacological potency decreases.3 Variability in NTG potency also has been reported with different ambient temperatures.4 Because the chemical efficacy of NTG is often critical in the prehospital management of patients who have chest pain or heart failure, and because temperatures to which NTG tablets are exposed are variable, we evaluated the actual amount of active NTG present in tablets sampled from paramedic vehicles in the Los Angeles area. In Los Angeles County, paramedics normally carry NTG in small brown glass bottles of 25 tablets (400 p,g) per bottle. After 3 months, or when the number of tablets in the bottle falls below five, paramedics are instructed to resupply with a new bottle of 25 tablets. Between October 1986 and March 1987, bottles of NTG tablets were removed from 18 para681
Reference 1. Svenson J: Obtundation in the elderly patient: Presentation of a drug overdose. Am J Emerg Med 1987;5:524-528
The author replies:-The admitting diagnosis of the patient in my article was “cerebrovascular accident,” rather than “cardiovascular accident,” and I apologize for not correcting the error during proofreading. I agree with Dr Little that one is hard pressed to fully explain this patient’s symptoms on the basis of a cerebrovascular accident. Certainly brainstem infarctions can lead to alterations in consciousness, but these are usually overshadowed by other, more dramatic, neurological signs. Perhaps the admitting diagnosis should have been “lethargy-? etiology.” Although the choice of admitting diagnosis by her attending physician may be questionable, neither I nor the journal have any control over the facts. I would emphasize that one of the major points of my article is to consider other diagnoses (for example, occult drug ingestion) in the elderly when the clinical data do not quite fit into some well-defined syndrome. I thank Dr Little for his comments. JAMESSVENSON,MD Madison, Wisconsin
The American Journal of Emergency Medicine invites correspondence, commentary, and criticism in the form of letters to the editor. Please address correspondence to The Editor: The American Journal of Emergency Medicine, 3800 Reservoir Rd, NW, Washington, DC 20007.
PULSATILE TINNITUS DURING A VALSALVA MANEUVER IN A PATIENT WITH WOLFF-PARKINSON-WHITE SYNDROME To the Editor:-Wolff-Parkinson-White (WPW) syndrome, a common cause of paroxysmal supraventricular tachycardia, was first described in 1930.’ Patients with this disease may have no complaints or may complain of palpitations, dyspnea, or chest pain. In those who are symptomatic, many have learned to end their discomfort by self-converting the tachycardia back into a normal sinus rhythm through the use of carotid massage or the Valsalva maneuver. Although the use of the Valsalva maneuver has frequently been recorded to be of benefit in these patients, the literature reveals no reports of pulsatile tinnitus occurring during the maneuver. We recently treated a patient with WPW syndrome whose conversion from a supraventricular tachycardia to a normal sinus rhythm was manifested by pulsatile tinnitus during his use of the Valsalva maneuver. A 63-year-old Hispanic man presented to the emergency department (ED) with a chief complaint of chest pain. The pain had begun earlier that day, was not associated with activity, and radiated into the left neck and arm. The pain lasted for approximately two hours, but was not present at the time of examination by the medical student. He reported having similar episodes of chest pain once every 3 to 4 months over the past 7 years. He noted that he could make the chest pain go away by taking rapid, forceful deep breaths, but when he did so he heard a rhythmic “clicking” in his ears. The pain would cease immediately after this measure. He denied any other cardiac or pulmonary symptomatology; his history was negative for palpitations, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, or dyspnea on exertion. His past history was remarkable only for a left ankle fracture and a stab wound to the abdomen. He took no medications at home and had no known allergies. Family history was unremarkable, but he acknowledged a one pack per day smoking history and an alcohol intake of many cans of beer per day, both of an unknown duration. On examination, he was a slightly obese, ill-kempt man who was alert, cooperative, and in no acute distress. The odor of alcohol was present on his breath. Initial vital signs showed a pulse of 88, respiratory rate 20, BP 124/70, and temperature of 95S”F. Examination of the head, ears, eyes, nose, and throat was unremarkable. The neck was supple with no adenopathy, jugular venous distension, or carotid bruits noted. Carotid upstroke was good bilaterally. The chest was clear to auscultation. Cardiovascular examination revealed a regular rate and rhythm with no murmur, S3, or S4 noted. Abdominal examination was benign. The extremities were without cyanosis or edema, and pulses were good throughout. The neurological examination was grossly intact. The diagnosis of unstable angina, rule out myocardial infarction, was entertained in light of the patient’s history of
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
W Volume
6, Number
chest pain. An intravenous (IV) line was established and oxygen was administered by nasal cannula. Initial laboratory values showed a WBC count of 7,500 with 39 polycites, 54 lymphocytes, 5 monocytes, 1 eosinophil, and 1 basophil; hemoglobin was 15.0 g/dL, hematocrit 44%, platelets 376,000, and RBC indices (mean corpuscular volume, mean corpuscular hemaglobin, and mean corpuscular hemaglobin concentration) were within normal limits. Chemistry revealed: sodium, 141; potassium, 3.3; chloride, 108; CO,, 21; BUN, 5; creatinine, 0.9; and glucose, 125. Creatinine phosphokinase was 148, lactate dehydrogenase was 147, and SGOT was 34. Room air arterial blood gases showed a pH of 7.39, p0, of 72 mmHg, and pC0, of 38 mmHg. Hemoglobin saturation was 95%. The ECG showed a normal sinus rhythm at a rate of 100 with left axis deviation. No evidence of ischemia, infarction, or conduction abnormality was noted. The medicine service was notified of a consultation for admission to rule out myocardial infarction. The patient was resting comfortably in the treatment area, his cardiac rhythm being monitored by telemetry. A few minutes later, the ED attending physician noted that the patient had initiated a supraventricular tachycardia with a rate near 150 beats per minute. The physician again evaluated the patient, who had now developed the sudden onset of chest pain. Vital signs revealed a pulse increase to 160 beats per minute, and systolic BP had fallen to 80 mmHg. The patient was placed in the Trendelenberg position and the BP increased to 90 mmHg systolic, without a change in pulse rate. The patient was asked to reproduce what he usually did at home to make the pain stop. The patient performed several repetitions of forceful inspiration and exhalation, which were recognized by the attending physician as a Valsalva maneuver. However, the pain continued and 2.5 mg IV verapamil were administered. The patient was asked to repeat the Valsalva maneuver. This time he reported hearing a rhythmic “clicking” sound in both ears, and as he did so the pain abruptly ceased. A review of the monitor strip taken during this episode demonstrated clearly the conversion of the patient’s tachycardia to a normal sinus rhythm (Fig 1). The patient was admitted to the medicine service with a diagnosis of supraventricular tachycardia. Myocardial infarction was ruled out through serial ECGs and cardiac en-
FIGURE 1. maneuver.
Monitor strip revealing conversion of a supraventricular
6 n November
1988
zyme determinations. Cardiology consultation was obtained, and it was felt that the patient had a WPW preexcitation syndrome using an accessory conduction pathway on the left side of the heart. It was noted that the findings suggestive of WPW syndrome were rate-dependent and seen only on ECGs performed at slower heart rates. These findings were not evident on the initial tracing done in the ED. Twentyfour-hour Holter monitoring confirmed the presence of delta waves at slower heart rates, and a three-minute run of SVT, thought to involve the left atrioventricular bypass tract in a retrograde fashion, was recorded. The patient did well throughout his hospital stay and was discharged to home on Inderal LA, 80 mg each morning. He was noted to be doing well on subsequent visits to the outpatient internal medicine clinic. In the case of this patient, the use of the Valsalva maneuver had been self-taught as a means of ending each episode of tachycardia (manifested clinically by chest pain). Of interest is the association between the use of this maneuver and the repetitive clicking sound he heard in his ears, a perception that might best be considered as pulsatile tinnitus. Although pulsatile tinnitus has been well described in the otologic literature,2.3 it has received scant notice elsewhere, and in no instance before has it been associated with the use of the Valsalva maneuver. Pulsatile tinnitus has been described as the hearing of rhythmic sounds that are synchronous with the pulse. The causes of pulsatile tinnitus may be divided into two groups. Those due to lesions of the arterial system of the head and neck include arteriovenous malformations, arterioarterial anastomoses, and intraluminal irregularities of the carotids (such as arteriosclerosis and fibromuscular dysplasia). Causes of pulsatile tinnitus of nonarterial origin include cervical venous hums, cardiac murmurs, abnormalities of the jugular bulb, increased intracranial pressure, and neoplasms of the middle ear and temporal bone.2 The management of pulsatile tinnitus in the ED includes a careful history, especially for the presence of decreased hearing, headache, or other neurological symptoms, and a meticulous physical examination to include auscultation of the carotids and auricular region. cardiovascular examination, ophthalmoscopy, and tympanoscopy. Referral to an otolaryngologist is essential. Further workup may include audiologic assessment,
tachycardia to a normal sinus rhythm during performance
of the Valsalva
CORRESPONDENCE
computed
tomography
of the head, and carotid or cerebral
angiography . HOWARD RODENBERG,MD MATTHEW GRATTON, MD
Truman Medical Center Kansas City, Missouri
References Wolff L, Parkinson J, White PD: Bundle branch block with short R-P interval in healthy young people prone to paroxysmal tachycardia. Am Heart J 1930;5:665 Levine SB, Snow JB Jr: Pulsatile tinnitus. Laryngoscope 1967;97:401-406 Sila CA, Furlan AJ, Little JR: Pulsatile tinnitus. Stroke 1987;18:252-256
POVIDONE-IODINE SOLUTIONS IN TRAUMATIC WOUND PREPARATION To the Editor:-AJEM published a letter by Michael S. Oberg, MD entitled “Povidone-Iodine Solutions in Traumatic Wound Preparation,“’ which contained opinions based on a very limited number of references. In addition, some of the references quoted have little or no relevance to the practical and proper use of povidone-iodine. Dr Oberg declares the data to be conflicting, yet reaches conclusions and a recommendation. The reason for conflicting data derives from the difficulties encountered in the studies reported rather than the failure of the agent. Numerous studies which are not cited conclusively demonstrate the usefulness of povidone-iodine solution in the management of wounds.‘-” KENNETH G. ROTHWELL, MD
Easton, Connecticut
References 1. Oberg MS: Povidone-iodine solutions in traumatic wound preparation. Am J Emerg Med 1987;5:553-555 (letter) 2. Garnes AL, Davidson E, Taylor LE, et al: Clinical evaluation of povidone-iodine spray in surgical practice. Am J Surg 1959;97:49-53 3. Lee BY, Trainor FS, Thoden WR: Topical application of povidone-iodine in the management of decubitis and stasis ulcers. J Am Geriatr Sot 1979;27:302-306 4. Kwaan JHM, Connolly JE: Successful management of prosthetic graft infection with continuous povidone-iodine irrigation. Arch Surg 1981;116:716-720 5. Morgan WJ: The effect of povidone-iodine aerosol spray on superficial wounds. Br J Clin Pratt 1979;33:109-110 6. Gilgore A: The use of povidone-iodine in the treatment of infected cutaneous ulcers. Curr Ther Res 1978;24:843-848 7. Stefanides MM, Copeland DE, Kominos SD, et al: In vitro penetration of topical antiseptics through eschar of burn patients. Ann Surg 1976;183:358-364 8. Wynn-Williams D, Monballiu G: The effects of povidoneiodine in the treatment of burns and traumatic losses of skin. Br J Plast Surg 1965;18:146-150 9. Connell JF Jr, Rousselet LM: Povidone-iodine: Extensive surgical evaluation of a new antiseptic agent. Am J Surg 1964;108:849-855 10. Linkner LM, Cloud DT, Trump DS, et al: Prevention of bac-
terial growth and local infection in burn wounds. J Ped Surg 1972;7:310-314 11. Georgide NG, Matton GE, Kessel FV: Facial burns. Plast Reconstr Surg 1962;29:648-657
The author replies:-1 have read Dr Rothwell’s letter and it is not clear to me that he read either the title or the body of my correspondence. Nor is it clear to me what his interest in the subject is. My interest is as an emergency physician who had to deal with one of those mundane but important issues that face us all in the emergency department (ED). My letter dealt with the use of povidone-iodine solutions on acute traumatic wounds in the ED, ie, lacerations. I offered it in the hope that other emergency physicians who have to deal with this issue might find it helpful. I fail to see that the references Dr Rothwell offers on the treatment of decubitus ulcers, stasis ulcers, cutaneous ulcers, penetration through bum eschar, and chronic bum care have much relevance to treatment of acute lacerations. Many of the references he cites were unearthed in my search but not used for the reasons noted or because some had been superseded by more recent studies. Elsewhere in the letter, I stated that povidoneiodine is a valuable agent (our own hospital uses it by the gallon); I just question its value in this context. I feel that my letter fairly summarized the recent and still somewhat sparse literature on this subject. The results are indeed conflicting and the conclusions I reached are clearly labeled as my own beliefs. I stand by the letter as written. Thank you for this opportunity to reply. MICHAEL S. OBERG, MD
Arlington, Texas
CHEMICAL STABILITY OF SUBLINGUAL NITROGLYCERIN TABLETS CARRIED ON PARAMEDIC VEHICLES To the Editor:-Sublingual nitroglycerin (NTG) has long been used for the treatment of patients with cardiac chest pain. Although its predominant action is as a venodilator effectively reducing cardiac preload, NTG also relaxes peripheral vascular smooth muscle, producing a fall in cardiac afterload as well.’ Both atherosclerotic and normal coronary arteries dilate following NTG administration.’ These vascular effects are the rationale for the administration of sublingual NTG tablets in patients experiencing angina pectoris, myocardial infarction, and acute pulmonary edema during the prehospital phase of illness. Upon exposure to air, NTG tablets begin to degrade, and their pharmacological potency decreases.3 Variability in NTG potency also has been reported with different ambient temperatures.4 Because the chemical efficacy of NTG is often critical in the prehospital management of patients who have chest pain or heart failure, and because temperatures to which NTG tablets are exposed are variable, we evaluated the actual amount of active NTG present in tablets sampled from paramedic vehicles in the Los Angeles area. In Los Angeles County, paramedics normally carry NTG in small brown glass bottles of 25 tablets (400 p,g) per bottle. After 3 months, or when the number of tablets in the bottle falls below five, paramedics are instructed to resupply with a new bottle of 25 tablets. Between October 1986 and March 1987, bottles of NTG tablets were removed from 18 para681