- Email: [email protected]
Ultrasound as a diagnostic tool
398
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume
10, Number
4 l July 1992
FIGURE 2. The computed tomographic scan, taken 4 days after the surgical repair of the carotideal dissection, shows a wide left parietal hypodensity.
References 1. Mokkri B, Piepgras DG, Wayne Houser 0: Traumatic dissections of the extracranial carotid artery. J Neurosurg 1988;68: 189-197 2. Davis JW, Holbrook TI, Hoyt DB, et al: Blunt carotid artery dissection: Incidence, associated injuries, screening and treatment. J Trauma 1990:30(12):1514-1517 3. Perry 0, Snyder WH; Thal ER: Carotid artery injuries caused by blunt trauma. Ann Surg 1980;192(1):74-77 4. Welling RE, Saul TG, Tew JM, et al: Management of blunt injury to the internal carotid artery. J Trauma 1987;27(11):12211226 5. Fabian TC, George SM, Croce MA, et al: Carotid artery trauma: Management based on the mechanism of action. J Trauma 1990;30(8):953-963 6. Watrdige CB, Mulhbauer MS, Lowery RD: Traumatic carotid artery dissection: Diagnosis and treatment. J Neurosurg 1989;71:854-857 7. Trust Study Group: Randomized, double blind, placebo controlled trial of nimodipine in acute stroke. Lancet 1990;336: 1205-l 209
ULTRASOUND AS A DIAGNOSTIC TOOL To the Editor:--We applaud the efforts of Amitai et al to apply ultrasound as a toxicology diagnostic tool; however, we encourage caution in the application of ultrasound for this purpose and several caveats must be considered. First, the ultrasound device used, an Acuson 128 (Acuson, Mountain View, CA) is a large, expensive, nonportable unit with a linear array transducer that will realistically be found only in departments of radiology. This implies that patient transport out of the emergency department will be necessary (not an ideal practice in patients with acute drug ingestion), and also that the results of the imaging attempts cannot be generalized to the less sophisticated scanners likely to be available to the emergency physician. Even with the advantages of excellent equipment and trained ultrasound personnel, it is not at all clear that ultrasound has much to offer the clinical management of the poisoned patient, even the small minority ingesting sustained release preparation. The fact that four such pills were detected in the stomach of volunteers known to have ingested those products in no way indicates that they would be
399
CORRESPONDENCE
consistently detected in actual patients in whom the history of ingestion is far less certain. The authors have not attempted to extrapolate their data to other medications and very prudently advise the reader regarding the limitations of ultrasound as a toxicology diagnostic tool. Particularly, the clinician should consider that there is a significant delay between the time of the ingestion and the patient’s ultimate arrival in the emergency department. Typically that delay will be 1 to 3 hours or more, during which time gastric dissolution of the ingested medication may occur, resulting in false-negative results due to the lack of a sonographically definable target. Therefore, negative results should not be considered as confirmatory evidence that an ingestion did not occur or that gastric decontamination with activated charcoal or gastric lavage is of no value. A greater potential application of this technique which may merit study, is the identification of drug bezoars which, through continuous absorption, can produce toxicity. EDWARD P. KRENZELOK, PHARMD MICHAEL B. HELLER, MD University of Pittsburgh, School of Medicine Pittsburgh, PA The authors reply-Drs Krenzelok and Heller bring up several cogent aspects to the application of ultrasonography to drug ingestion and we appreciate their remarks. Our study represents a first step in exploring the potential use of ultrasound in the detection of pills in the stomach of subjects following acute ingestion; there is obviously a need for more research in this field. The Acusan 128 ultrasound unit (Acuson Computed Sonography, Mountain View, CA) used in our study is capable of being moved out of the radiology department and is routinely used for portable studies. In fact the examination reported in our study was done portably in the emergency department. Almost all modem real-time ultrasound units have adequate resolution and only require medium frequency transducers in the 3 to 5 mHz (sector or linear) range to image the stomach and its contents. These transducers are standard on almost all ultrasound units. One of the objectives stated in our paper was to study the limitations of ultrasound in detecting pills in the stomach. While size of the pill does not appear to be a limiting variable, dissolution time is a major factor. We agree with Drs Krenzelok and Heller that the variable detection by ultrasound of immediate release medication restricts the number of potential patients for such study. Nevertheless, the growing trend in the pharmaceutical industry to develop new sustained-release formulations, and the complexity of the management of patients with overdose of such drugs, may well increase the use of ultrasound in the future. Prospective studies are indeed required to determine the limits of this capability. We agree that nonvisualization can be consistent with drug ingestion and this certainly merits further study. With increased availability of ultrasound units in emergency departments and improved familiarity of emergency physicians with this technique, ultrasonography can become a useful ancillary tool in the evaluation of the poisoned patient. As Drs Krenzelok and Heller note, drug bezoars should be easily detected by ultrasonography. Moreover, this technique can provide information on incidence of bezoar formation, and help identify body stuffers and body packers. As the use of ultrasonography expands, more uses of this tool in toxicology will be identified.
JERROLDB. LEIKIN, MD BRUCE SILVER, MD
HENFUFRISCHER, MD, PHD Rush-Presbyterian-St Chicago, IL
Luke’s Medical Center
TWITCHING AS A MANIFESTATION OF OCCULT UREMIA To the Editor:-The clinical findings of the uremic syndrome are typically subtle. Progressive weakness, easy fatigability, lethargy, anorexia, vomiting, hiccup, and itching are common initial manifestations of the uremic syndrome. Recently, we cared for a patient that had an unusual initial presentation of uremia. A 57-year-old man presented to the emergency department with complaints of “whole body twitching.” He had been in his usual state of health until 1 week prior to admission when he developed chills, sneezing, and a low-grade fever. He was seen by his personal physician who gave him an injection of Phenergan 25 mg (promethazine hydrochloride; Wyeth-Ayerst Laboratories, Philadelphia, PA). This was followed by 3 days of epigastric pain and “whole body twitching,” which initially was thought to be related to his Phenergan administration. His physician consequently administered oral Benadryl (diphenhydramine hydrochloride; Parke-Davis, Morris Plains, NJ) and advised rest. Eight hours following discharge from the physician’s office, the patient’s twitching returned, and he presented to our emergency department. There was no history of any chemical exposure. He denied the use of any other medications or illegal drugs, and had no significant past medical history. On initial physical examination his blood pressure was 130/70 mm Hg, heart rate 68/min, respirations 16/min, and body temperature was 37°C. He had generalized movements with a frequency of 10 to 15 per minute. There was no evidence of cardiopulmonary decompensation and his neurologic examination was otherwise completely unremarkable. Laboratory data obtained in the ED revealed the following levels: sodium, 145 mmol/L; potassium, 4.7 mmol/L; chloride, 113 mmoVL; bicarbonate, 12 mmol/L; blood urea nitrogen, 55.7 mmol/L (156 mg/ dL); creatinine, 1,220 FmollL (13.8 mg/dL); glucose, 6.2 mmoVL (112 mg/dL); and phosphorus, 3 mmol/L (9.3 mg/dL). Arterial blood gases on room air revealed a pH 7.19, pcoZ 26 torr, po, 99 torr. The patient was admitted to the hospital for emergent hemodialysis. Further investigation revealed IgA nephropathy. Since then the patient has had only two episodes of “twitching,” each of them occurring when he missed his hemodialysis. Twitching is defined as a momentary spasmodic contraction of a muscle fiber.’ To our knowledge, the association of this symptom and uremia has been described only once, in a 74-year-old woman with chronic renal failure, who had an idiosyncratic reaction to ciprofloxacin and experienced generalized myoclonus and muscle twitching with evidence of worsening of her renal function.2 JOSEPHVARON, MD Baylor College of Medicine Houston, TX HEDAYATOLLAH ZAGHI, MD University of Washington Seattle, WA GEORGEL. STERNBACH,MD, FACEP Stanford University Medical Center Stanford, CA
References YONA AWITAI, MD Hadassah University Hospital Chicago, IL
1. Stedman’s Medical Dictionary Williams 8. Wilkins, 1990, p 1656
(ed 25).
Baltimore,
MD,
2. Schwartz MT, Calvert JF: Potential neurologic toxicity related to ciprofloxacin. Drug Intel1 Clin Pharm 1990;24:136-140
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume
10, Number
4 l July 1992
FIGURE 2. The computed tomographic scan, taken 4 days after the surgical repair of the carotideal dissection, shows a wide left parietal hypodensity.
References 1. Mokkri B, Piepgras DG, Wayne Houser 0: Traumatic dissections of the extracranial carotid artery. J Neurosurg 1988;68: 189-197 2. Davis JW, Holbrook TI, Hoyt DB, et al: Blunt carotid artery dissection: Incidence, associated injuries, screening and treatment. J Trauma 1990:30(12):1514-1517 3. Perry 0, Snyder WH; Thal ER: Carotid artery injuries caused by blunt trauma. Ann Surg 1980;192(1):74-77 4. Welling RE, Saul TG, Tew JM, et al: Management of blunt injury to the internal carotid artery. J Trauma 1987;27(11):12211226 5. Fabian TC, George SM, Croce MA, et al: Carotid artery trauma: Management based on the mechanism of action. J Trauma 1990;30(8):953-963 6. Watrdige CB, Mulhbauer MS, Lowery RD: Traumatic carotid artery dissection: Diagnosis and treatment. J Neurosurg 1989;71:854-857 7. Trust Study Group: Randomized, double blind, placebo controlled trial of nimodipine in acute stroke. Lancet 1990;336: 1205-l 209
ULTRASOUND AS A DIAGNOSTIC TOOL To the Editor:--We applaud the efforts of Amitai et al to apply ultrasound as a toxicology diagnostic tool; however, we encourage caution in the application of ultrasound for this purpose and several caveats must be considered. First, the ultrasound device used, an Acuson 128 (Acuson, Mountain View, CA) is a large, expensive, nonportable unit with a linear array transducer that will realistically be found only in departments of radiology. This implies that patient transport out of the emergency department will be necessary (not an ideal practice in patients with acute drug ingestion), and also that the results of the imaging attempts cannot be generalized to the less sophisticated scanners likely to be available to the emergency physician. Even with the advantages of excellent equipment and trained ultrasound personnel, it is not at all clear that ultrasound has much to offer the clinical management of the poisoned patient, even the small minority ingesting sustained release preparation. The fact that four such pills were detected in the stomach of volunteers known to have ingested those products in no way indicates that they would be
399
CORRESPONDENCE
consistently detected in actual patients in whom the history of ingestion is far less certain. The authors have not attempted to extrapolate their data to other medications and very prudently advise the reader regarding the limitations of ultrasound as a toxicology diagnostic tool. Particularly, the clinician should consider that there is a significant delay between the time of the ingestion and the patient’s ultimate arrival in the emergency department. Typically that delay will be 1 to 3 hours or more, during which time gastric dissolution of the ingested medication may occur, resulting in false-negative results due to the lack of a sonographically definable target. Therefore, negative results should not be considered as confirmatory evidence that an ingestion did not occur or that gastric decontamination with activated charcoal or gastric lavage is of no value. A greater potential application of this technique which may merit study, is the identification of drug bezoars which, through continuous absorption, can produce toxicity. EDWARD P. KRENZELOK, PHARMD MICHAEL B. HELLER, MD University of Pittsburgh, School of Medicine Pittsburgh, PA The authors reply-Drs Krenzelok and Heller bring up several cogent aspects to the application of ultrasonography to drug ingestion and we appreciate their remarks. Our study represents a first step in exploring the potential use of ultrasound in the detection of pills in the stomach of subjects following acute ingestion; there is obviously a need for more research in this field. The Acusan 128 ultrasound unit (Acuson Computed Sonography, Mountain View, CA) used in our study is capable of being moved out of the radiology department and is routinely used for portable studies. In fact the examination reported in our study was done portably in the emergency department. Almost all modem real-time ultrasound units have adequate resolution and only require medium frequency transducers in the 3 to 5 mHz (sector or linear) range to image the stomach and its contents. These transducers are standard on almost all ultrasound units. One of the objectives stated in our paper was to study the limitations of ultrasound in detecting pills in the stomach. While size of the pill does not appear to be a limiting variable, dissolution time is a major factor. We agree with Drs Krenzelok and Heller that the variable detection by ultrasound of immediate release medication restricts the number of potential patients for such study. Nevertheless, the growing trend in the pharmaceutical industry to develop new sustained-release formulations, and the complexity of the management of patients with overdose of such drugs, may well increase the use of ultrasound in the future. Prospective studies are indeed required to determine the limits of this capability. We agree that nonvisualization can be consistent with drug ingestion and this certainly merits further study. With increased availability of ultrasound units in emergency departments and improved familiarity of emergency physicians with this technique, ultrasonography can become a useful ancillary tool in the evaluation of the poisoned patient. As Drs Krenzelok and Heller note, drug bezoars should be easily detected by ultrasonography. Moreover, this technique can provide information on incidence of bezoar formation, and help identify body stuffers and body packers. As the use of ultrasonography expands, more uses of this tool in toxicology will be identified.
JERROLDB. LEIKIN, MD BRUCE SILVER, MD
HENFUFRISCHER, MD, PHD Rush-Presbyterian-St Chicago, IL
Luke’s Medical Center
TWITCHING AS A MANIFESTATION OF OCCULT UREMIA To the Editor:-The clinical findings of the uremic syndrome are typically subtle. Progressive weakness, easy fatigability, lethargy, anorexia, vomiting, hiccup, and itching are common initial manifestations of the uremic syndrome. Recently, we cared for a patient that had an unusual initial presentation of uremia. A 57-year-old man presented to the emergency department with complaints of “whole body twitching.” He had been in his usual state of health until 1 week prior to admission when he developed chills, sneezing, and a low-grade fever. He was seen by his personal physician who gave him an injection of Phenergan 25 mg (promethazine hydrochloride; Wyeth-Ayerst Laboratories, Philadelphia, PA). This was followed by 3 days of epigastric pain and “whole body twitching,” which initially was thought to be related to his Phenergan administration. His physician consequently administered oral Benadryl (diphenhydramine hydrochloride; Parke-Davis, Morris Plains, NJ) and advised rest. Eight hours following discharge from the physician’s office, the patient’s twitching returned, and he presented to our emergency department. There was no history of any chemical exposure. He denied the use of any other medications or illegal drugs, and had no significant past medical history. On initial physical examination his blood pressure was 130/70 mm Hg, heart rate 68/min, respirations 16/min, and body temperature was 37°C. He had generalized movements with a frequency of 10 to 15 per minute. There was no evidence of cardiopulmonary decompensation and his neurologic examination was otherwise completely unremarkable. Laboratory data obtained in the ED revealed the following levels: sodium, 145 mmol/L; potassium, 4.7 mmol/L; chloride, 113 mmoVL; bicarbonate, 12 mmol/L; blood urea nitrogen, 55.7 mmol/L (156 mg/ dL); creatinine, 1,220 FmollL (13.8 mg/dL); glucose, 6.2 mmoVL (112 mg/dL); and phosphorus, 3 mmol/L (9.3 mg/dL). Arterial blood gases on room air revealed a pH 7.19, pcoZ 26 torr, po, 99 torr. The patient was admitted to the hospital for emergent hemodialysis. Further investigation revealed IgA nephropathy. Since then the patient has had only two episodes of “twitching,” each of them occurring when he missed his hemodialysis. Twitching is defined as a momentary spasmodic contraction of a muscle fiber.’ To our knowledge, the association of this symptom and uremia has been described only once, in a 74-year-old woman with chronic renal failure, who had an idiosyncratic reaction to ciprofloxacin and experienced generalized myoclonus and muscle twitching with evidence of worsening of her renal function.2 JOSEPHVARON, MD Baylor College of Medicine Houston, TX HEDAYATOLLAH ZAGHI, MD University of Washington Seattle, WA GEORGEL. STERNBACH,MD, FACEP Stanford University Medical Center Stanford, CA
References YONA AWITAI, MD Hadassah University Hospital Chicago, IL
1. Stedman’s Medical Dictionary Williams 8. Wilkins, 1990, p 1656
(ed 25).
Baltimore,
MD,
2. Schwartz MT, Calvert JF: Potential neurologic toxicity related to ciprofloxacin. Drug Intel1 Clin Pharm 1990;24:136-140