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Carotid artery dissection and stroke caused by airbag injury
372
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 20, Number 4 • July 2002
In the present case we exclude relationship between anaphylactic shock and diuretics, because this patient was under regular therapy with hydrochlorothiazide, in the absence of any side effect. A sulphonamide cross-reaction 8 was not shown because the patient did not accept the skin reaction test. The cause of drug-induced pulmonary edema remains unknown but, recently, an immunologically mediated mechanism has been suggested.I° MASSIMO GALLERANI,MD NADIA MANZOLI,MD RENATOFELLIN, MD
Section of Internal Medicine H MICHELE SIMONATO
Section of Clinical Pharmacology Department of Clinical and Experimental Medicine, University of Ferrara, Ferrara, Italy CARLOORZINCOLO,MD Department of Radiology St. Anna Hospital Ferrara, Italy FIGURE 2. symptoms.
Chest CT scan performed 3 hours after occurrence of
were normal. The patient recovered fully, and was discharged 5 days later. Follow-up at 15, 30 days, and 6 months confirmed the complete recovery, with normal ECG and echocardiogram. The patient refused a skin reaction test to investigate hypersensivity to sulphonamide. In the present case clinical patterns, clinical ongoing, radiological findings confirmed acute puhnonary edema and excluded adult respiratory distress syndrome (ARDS) 2 and a primitive cardiac cause. In fact, preoperative investigations did not reveal heart diseases; furthermore, no sign of heart failure occurred during hospital admission nor in the follow-up. The relationship between anaphylactic shock and acetazolamide seems highly probable, considering the short time between drug assumption and onset of symptoms (about 30 minutes) and the absence of previous diseases to which symptoms could be related. 3 The patient was not previously treated with acetazolamide. Acetazolamide is a carbonic anhydrase inhibitor diuretic, and the prototype of a family of sulphonamide-derived drugs, which includes diclorphenamide and methazolamide. A nonsubstituted sulphonamide group is present in all of these drugs. Nowadays, the clinical use of acetazolamide is very limited. Its principal uses are in the preoperative treatment of closed angle glaucoma and continuative therapy of open angle glaucoma. Acetazolamide, like other sulphonamides, may cause bone marrow depression, skin toxicity, and allergic reactions in patients hypersensitive to sulphonamides. 4, 5 Serious anaphylactic reactions to acetazolamide are infrequent. Peralta et al 6 reported a 66-yearold woman who developed anaphylactic shock associated with laryngeal edema, respiratory distress syndrome, and death after ingestion of 250 mg of 2acetazolamide. Tzanakis et aF described a 70-year-old man with sulphonamide hypersensitivity, who presented acute respiratory failure 30 minutes after taking 250 mg of acetazolamide. Recently, Gerhards et al s reported a 66-year-old female who developed irreversible anaphylactic shock with massive pulmonary edema after assumption of acetazolamide. The investigators hypothesized that this adverse effect was attributable to cross-reaction with snlphonamide. Riquelme et al 9 described a 33-year-01d man who presented hypotension and acute heart failure 30 minutes after acetazolamide assumption. The investigators hypothesized an etiopathogenetic mechanism similar to thiazide diuretics hypersensitivity.
References 1. DRUGDEX System: Hutchison TA, Shahan DR. Anderson ML (eds): DRUGDEX System. MICROMEDEX, Inc., Greewood Village, CO vol 108, 03/15/2001 2. Gluecker T, Capasso P, Schnyder P, et al: Clinical and radiologic features of pulnomary edema. Radiographics 1999;19: 1507-31 3. Karch FE, Lasagna L: Adverse drug reactions. A critical review. JAMA 1975;234:1236-41 4. Begg IS, Cottle RW: Epidemiological approach to open-angle gglaucoma: 2. Survival analysis of adverse reactions. Report of the Canadian Ocular Adverse Drug Reaction Registry Program. The Collaborative Glaucoma Study Group. Can J Ophthalmol 1989;24: 15-19 5. Reyes E, Izquierdo NJ, Blasini M: Adverse drugs reactions associated with glaucoma medications. Bol Asoc Med P R 1997; 89:51-5 6. Peralta J, Abelairas J, Fernandez-Guardiola J: Anaphylactic shock and death after oral intake of acetazolamide. Am J Ophtalmol 1992; 114:367 7. Tzamakis N, Metzidaki G, Thermos K, et al: Anaphylactic shock after a single oral intake of acetazolamide. Br J Ophtalmol 1998;82:584 8. Gerhards LJ, van Arnhem AC, Holman ND, et al: Fatale anafylactische reactie na inname van acetazolamede (Diamox). Ned Tijdschr Geneeskd 2000;144:1228-30 9. Riquelme JP, Riquelme CP, Colome FC: Edema agudo de pulm6n asociado a la ingesta de acetazolamida. Med Clin (Barc) 1987;89:353 10. Bernal C, Patarca R: Hydrochlorothiazide-induced pulmonary edema and associated immunologic changes. Ann Pharmacother 1999;33:172-4
CAROTID ARTERY DISSECTION AND STROKE CAUSED BY AIRBAG INJURY To the Editor:--We report an unusual case of carotid dissection and stroke in a 53-year-old man injured in a motor vehicle accident (MVA). He sustained no apparent initial injury; the only direct impact came from a deployed airbag. Over the next 3 days he developed a right hemiplegia. He was found to have a left carotid artery dissection and middle cerebral aneurysm (MCA) distribu-
Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0024535.00/0 doi: 10.1053/ajem.2002.34193
• CORRESPONDENCE
tion stroke. This case shows the potential for delayed neurologic injury after airbag deployment in the absence of obvious immediate injury. The patient was a 53-year-old man without any significant past medical history who took no medications. He was 5'10" tall, muscular, and weighed 165 pounds. He was wearing a seat belt when the front of his vehicle struck a similar size car at approximately 30 mph causing steering wheel airbag deployment. He walked away from the accident without neurologic complaints; sustaining no apparent injury. On postaccident day 1 he complained of neck and chest pain as well as right hand numbness, the latter was fek by his private medical doctor to be cervical radiculopathy. The next day he noted right hand weakness and mild iight leg numbness. He awoke on postaccident day 3 with complete right hemiplegia. He was then hospitalized. The neurologic examination revealed a normal mental status without any evidence of aphasia. Cranial nerve examination was notable for right facial weakness (central type), without evidence of a Homer's Syndrome. Complete (0/5) paralysis of the right arm and leg was present. Sensation was fully intact in all 4 limbs and the face. General medical examination was unremarkable. Diffusion-weighted magnetic resonance imaging showed a large crescent-like defect in the distribution of the left MCA deep border zone area. Magnetic resonance angiography showed a normal left common carotid artery (CCA). Marked abnormal narrowing of the left cervical internal carotid artery (ICA) was observed just beyond the left CCA bifurcation (Fig I). Minimal intracranial flow was seen in the precavernous, cavernous, and supraclinoid left ICA. Both anterior carotid arteries (ACAs) had normal blood flow; the right ICA via the anterior communicating artery supplied the left ACA. Extremely scant blood flow was noted in the left MCA distribution. The study was felt to represent dissection with clot formation. Chest radiograph showed a fracture of the proximal one-third of the sternum. Plain films and computed tomography of the C Spine
373
showed degenerative changes without soft tissue swelling, fracture, or dislocation. Laboratory studies were unremarkable. Treatment with heparin was initiated. He remained hospitalized for 13 days with no change in clinical status. Repeat magnetic resonance angiography studies failed to show lysis of the left ICA clot. He then began a gradual improvement, 6 weeks after the accident he was ambulating with a cane and able to raise his right arm to shoulder level. Carotid artery dissection as a direct result of airbag deployment has been reported in children. We found only 2 adult reports. The first case,~ a 39-year-old Irish man, presented with left hemiplegia and right parietal lobe stroke immediately after a MVA. Angiography revealed bilateral ICA dissection and previously undiagnosed fibromuscular dysplasia that was felt to be a predisposing condition. He improved with systemic heparinization. The second case, 2 a 44-year-old Australian woman, was neurologically intact on arrival in the ED but 40 minutes later developed a dense right hemiplegia and aphasia secondary to left ICA dissection. The risk factors for airbag injury include short stature, small body habitus, and positioning near the steering wheel. Previously reported neurologic air bag injuries include: 1. Fatal basilar skull fracture in a short forward-positioned 17-year-old girl. 3 The fracture line transected the carotid arteries bilaterally. 2. Fatal head injury 4 (adult). 3. Lethal cervical trauma with disruption of all ventral ligaments between the skull base and the first and second vertebrae, causing medullary destruction and diffuse axonal brain injury 5 (adult). 4. Cervical central spinal cord injury causing quadriplegia secondary to flexion-extension injury 6 (adult). 5. Closed head injuries v (child). This is the first North American case we are aware of carotid dissection as a direct result of airbag deployment. This case is unusual for several reasons. The patient was an averaged sized man with no known predisposing vascular abnormalities. The onset of the neurologic symptoms was delayed approximately 24 hours, with progression over 3 days. The initial symptoms masqueraded as cervical radiculopathy, unfortunately delaying diagnosis and treatment. MALCOLM GOTTESMAN,MD
Division of Neurology BRUCE SANDEROV,MD
Department of Emergency Medicine ORLANDOORTlZ, MD
Department of Radiology Winthrop University Hospital Mineola, NY
References
FIGURE 1. Dissection of the left cervical ICA with clot formation. The right ICA supplied both ACAs, scant MCA flow was present, most likely from collateral vessels.
1. Duncan MA, Dowd N, Rawluk D, et al: Traumatic bilateral internal carotid artery dissection following airbag deployment in a patient with fibromuscular dysplasia. Br J Anaesth 2000;85:476-8 2. Thomson BN, Davis SM: Carotid artery dissection: Another airbag injury. ANZ J Surg 2001 ;71:552-553 3. Perez J, Palmatier T: Air bag-related fatality in a short, forwardpositioned driver. Ann Emerg Med December 1996;28:722-724 4. Cunningham K, Brown TD, Gradwell E, et al: Airbag associated fatal head injury: case report and review of the literature on airbag injuries. J Accid Emerg Med 2000;17-139-42 5. Hart RA, Mayberry JC, Herzberg AM: Acute cervical spinal cord injury secondary to air bag deployment without proper use of lap or shoulder harnesses. J Spinal Disord 2000;13:36-8 6. Maxeiner H, Hahn M: Airbag-induced lethal cervical trauma. J Trauma 1997;42:1148-51
374
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 20, Number 4 • July 2002
7. Marshall KW, Koch BL, Egelhoff JC: Air bag-related deaths and serious injuries in children: injury patterns and imaging findings. Am J Neuroradiol 1998; 19:1599-607
SHOULD INTRAVENOUS CONTRAST BE USED IN PATIENTS RECEIVING METFORMIN To the Editor:--Daily practice for prescribing oral agents in medical treatment of adult-onset diabetes mellitus 1 typically fails to consider a practical issue which I believe necessary for consideration in emergency medicine practice. The issue is whether to use intravenous contrast agents in patients receiving metformin. In almost every hospital in this c0untry--including small community hospitals--radiologists refuse to use intravenous contrast in such diabetic patients, even in emergency situations. I believe that the following points should be considered in any review of medical treatment for Type 2, adult-onset diabetes mellitus.
1. The rate of lactic acidosis in diabetic patients who did not receive metformin was equivalent to the rate of lactic acidosis in diabetic patients receiving metformin, a This finding suggests both that metformin may not be a cause of increased lactic acidosis and that other conditions may be causing lactic acidosis in diabetic patients. However, this retrospective study merits further investigation. Nonetheless, according to the U.S. Food and Drug Administration (FDA), lactic acidosis in patients using mefformin is rare, occurring at a rate of 5 cases per 100,000 persons. 2 2. In nonurgent situations and when serum creatinine level is within nOlTnal range (<1.5 mg/dL; < 132.6 /xmolfL), intravenous contrast agents are not contraindicated. The previously recommended step of withholding administration of metformin for 48 hours before and after administration of the intravenous contrast agent is not necessary. The same strategy applies to emergency situations in which serum creatinine level is normal. Patients in such cases should be well hydrated before receiving the intravenous contrast agent. 3,4,5 3. In nonurgent cases when the patient is receiving metformin and has a creatinine level >1.5 mg/dL (>132.6 /xmol/L), metformin administration should be replaced by alternative diabetic control (eg, insulin) for a few days before the intravenous contrast study is done. 3,4,5 4. In urgent cases when the patient has a creatinine level > 1.5 mg/dL (>132.6 /xmol/L), metformin administration should be stopped, and steps (eg, intravenous hydration) should be taken to improve renal function. The intravenous contrast study should then be done but must be accompanied by close postprocedure monitoring and alternative diabetic control.3,4,5 I hope these points will be of interest both to general and to emergency practitioners and will be helpful. The author acknowledges the Medical Editing Department, Kaiser Foundation Research Institute, for providing editorial assistance.
RAJESHGUFrA,MD Department of Emergency Medicine Kaiser Permanente Medical Center Fresno, CA
References 1. Harrigan RA, Nathan MS, Beattie P: Oral agents for the treatment of type 2 diabetes mellitus: pharmacology, toxicity, and treatment. Ann Emerg Med 2001;38:68-78
Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0025535.00/0 doi:l 0.1053/ajem.2002.33953
2. Brown JB, Pedula K, Barzilay J, et al: Lactic acidosis rates in type 2 diabetes [published erratum appears in Diabetes Care 1998; 21:2203]. Diabetes Care 1998;21:1659-63 3. Nawaz S, Cleveland T, Gaines PA, et al: Clinical risk associated with contrast angiography in metformin treated patients: a clinical review. Clin Radiol 1998;53:342-4 4. McCartney MM, Gilbert FJ, Murchison LE, et al: Metformin and contrast media--a dangerous combination? Clin Radiol 1999;54: 29-33 5. Bush WA, Bettmann MA: Metformin (Glucophage) therapy and the risk of lactic acidosis. ACR Bull 1997;53:18-9
MASSIVE HEMOPTYSIS AND HEMOTHORAX CAUSED BY PLEUROPULMONARY ANGIOSARCOMA To the Editor:--Angiosarcoma involving the lung is a rare disorder and it is usually a metastatic disease. We reported a case of pleuropulmonary epithelioid angiosarcoma in a 36-year-old woman presenting simultaneously massive hemoptysis and hemothorax and rapidly radiographic change. The presentation was rarely entertained because of its infrequency and some differences compared with that of previously reported pulmonary angiosarcoma. A 36-year-old woman presented to ED because of intermittent hemoptysis for 2 months. Body weight loss and poor appetite were also complained. Bronchoscopy and brushing smear showed negative result at outside hospital 2 weeks ago. In the ED chest radiograph (Fig 1A) showed rfiild infiltrates in right upper lung field. Bronchoscopy showed some fresh blood in right main bronchus. Brushing and washing study showed no definite result. Unfortunately, progressive dyspnea and aggravated hemoptysis developed after admission. A series of chest radiographs also showed deterioration with progressive bilateral massive pleural effusion and opacity in both lungs (Fig 1B). Echo-guided thoracentesis showed hemothorax, but effusion study and pleural biopsy revealed no definite results. Subsequent high-resolution computed tomography of chest showed multiple focal consolidated patches in both lungs, small ill-defined nodules in bilateral upper lobes, and bilateral pleural effusion. Lung perfusion scan showed low probability of pulmonary embolism. Pulmonary artery angiogram showed no embolus or tumor in pulmonary trunk and their branches. The negative antinuclear antibody and rheumatoid factor, and rheumatological consultation did not favor vasculitis. The dyspnea and hemoptysis did not improve despite of steroid, antibiotics, anti-TB agents, oxygen therapy, and effusion drainage. The final diagnosis was obtained by video-assisted thoracoscopic surgery. The operative findings showed hematoma and fibrin coating on diaphragmatic surface, and no obvious diffuse pleural thickness or mass found. Decortication of left pleura, wedge resection of lingular lobe, pleural biopsy, and left lower lobe lung biopsy, were performed. The histology of pleural and lung biopsy showed epithelioid angiosarcoma. The immunohistochemical studies showed positive for the keratin marker CAM, the endothelial markers CD31, CD34 and factor VIII, and the aggressive clinical course markers P53 and Ki67. Cardiac echo, abdominal echo, and gynecologic echo were performed and did not show any tumor. After the diagnosis was made, she received chemotherapy and died of respiratory failure within 1 month. Epithelioid angiosarcoma of respiratory system is rare and needs to exclude metastasis. Thus far, 31 cases of pleural origin, 1 1 case of tracheal origin,2 1 case of pulmonary artery origin, 3 and 1 of
Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0026535.00/0 doi:10.1053/ajem.2002.34198
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 20, Number 4 • July 2002
In the present case we exclude relationship between anaphylactic shock and diuretics, because this patient was under regular therapy with hydrochlorothiazide, in the absence of any side effect. A sulphonamide cross-reaction 8 was not shown because the patient did not accept the skin reaction test. The cause of drug-induced pulmonary edema remains unknown but, recently, an immunologically mediated mechanism has been suggested.I° MASSIMO GALLERANI,MD NADIA MANZOLI,MD RENATOFELLIN, MD
Section of Internal Medicine H MICHELE SIMONATO
Section of Clinical Pharmacology Department of Clinical and Experimental Medicine, University of Ferrara, Ferrara, Italy CARLOORZINCOLO,MD Department of Radiology St. Anna Hospital Ferrara, Italy FIGURE 2. symptoms.
Chest CT scan performed 3 hours after occurrence of
were normal. The patient recovered fully, and was discharged 5 days later. Follow-up at 15, 30 days, and 6 months confirmed the complete recovery, with normal ECG and echocardiogram. The patient refused a skin reaction test to investigate hypersensivity to sulphonamide. In the present case clinical patterns, clinical ongoing, radiological findings confirmed acute puhnonary edema and excluded adult respiratory distress syndrome (ARDS) 2 and a primitive cardiac cause. In fact, preoperative investigations did not reveal heart diseases; furthermore, no sign of heart failure occurred during hospital admission nor in the follow-up. The relationship between anaphylactic shock and acetazolamide seems highly probable, considering the short time between drug assumption and onset of symptoms (about 30 minutes) and the absence of previous diseases to which symptoms could be related. 3 The patient was not previously treated with acetazolamide. Acetazolamide is a carbonic anhydrase inhibitor diuretic, and the prototype of a family of sulphonamide-derived drugs, which includes diclorphenamide and methazolamide. A nonsubstituted sulphonamide group is present in all of these drugs. Nowadays, the clinical use of acetazolamide is very limited. Its principal uses are in the preoperative treatment of closed angle glaucoma and continuative therapy of open angle glaucoma. Acetazolamide, like other sulphonamides, may cause bone marrow depression, skin toxicity, and allergic reactions in patients hypersensitive to sulphonamides. 4, 5 Serious anaphylactic reactions to acetazolamide are infrequent. Peralta et al 6 reported a 66-yearold woman who developed anaphylactic shock associated with laryngeal edema, respiratory distress syndrome, and death after ingestion of 250 mg of 2acetazolamide. Tzanakis et aF described a 70-year-old man with sulphonamide hypersensitivity, who presented acute respiratory failure 30 minutes after taking 250 mg of acetazolamide. Recently, Gerhards et al s reported a 66-year-old female who developed irreversible anaphylactic shock with massive pulmonary edema after assumption of acetazolamide. The investigators hypothesized that this adverse effect was attributable to cross-reaction with snlphonamide. Riquelme et al 9 described a 33-year-01d man who presented hypotension and acute heart failure 30 minutes after acetazolamide assumption. The investigators hypothesized an etiopathogenetic mechanism similar to thiazide diuretics hypersensitivity.
References 1. DRUGDEX System: Hutchison TA, Shahan DR. Anderson ML (eds): DRUGDEX System. MICROMEDEX, Inc., Greewood Village, CO vol 108, 03/15/2001 2. Gluecker T, Capasso P, Schnyder P, et al: Clinical and radiologic features of pulnomary edema. Radiographics 1999;19: 1507-31 3. Karch FE, Lasagna L: Adverse drug reactions. A critical review. JAMA 1975;234:1236-41 4. Begg IS, Cottle RW: Epidemiological approach to open-angle gglaucoma: 2. Survival analysis of adverse reactions. Report of the Canadian Ocular Adverse Drug Reaction Registry Program. The Collaborative Glaucoma Study Group. Can J Ophthalmol 1989;24: 15-19 5. Reyes E, Izquierdo NJ, Blasini M: Adverse drugs reactions associated with glaucoma medications. Bol Asoc Med P R 1997; 89:51-5 6. Peralta J, Abelairas J, Fernandez-Guardiola J: Anaphylactic shock and death after oral intake of acetazolamide. Am J Ophtalmol 1992; 114:367 7. Tzamakis N, Metzidaki G, Thermos K, et al: Anaphylactic shock after a single oral intake of acetazolamide. Br J Ophtalmol 1998;82:584 8. Gerhards LJ, van Arnhem AC, Holman ND, et al: Fatale anafylactische reactie na inname van acetazolamede (Diamox). Ned Tijdschr Geneeskd 2000;144:1228-30 9. Riquelme JP, Riquelme CP, Colome FC: Edema agudo de pulm6n asociado a la ingesta de acetazolamida. Med Clin (Barc) 1987;89:353 10. Bernal C, Patarca R: Hydrochlorothiazide-induced pulmonary edema and associated immunologic changes. Ann Pharmacother 1999;33:172-4
CAROTID ARTERY DISSECTION AND STROKE CAUSED BY AIRBAG INJURY To the Editor:--We report an unusual case of carotid dissection and stroke in a 53-year-old man injured in a motor vehicle accident (MVA). He sustained no apparent initial injury; the only direct impact came from a deployed airbag. Over the next 3 days he developed a right hemiplegia. He was found to have a left carotid artery dissection and middle cerebral aneurysm (MCA) distribu-
Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0024535.00/0 doi: 10.1053/ajem.2002.34193
• CORRESPONDENCE
tion stroke. This case shows the potential for delayed neurologic injury after airbag deployment in the absence of obvious immediate injury. The patient was a 53-year-old man without any significant past medical history who took no medications. He was 5'10" tall, muscular, and weighed 165 pounds. He was wearing a seat belt when the front of his vehicle struck a similar size car at approximately 30 mph causing steering wheel airbag deployment. He walked away from the accident without neurologic complaints; sustaining no apparent injury. On postaccident day 1 he complained of neck and chest pain as well as right hand numbness, the latter was fek by his private medical doctor to be cervical radiculopathy. The next day he noted right hand weakness and mild iight leg numbness. He awoke on postaccident day 3 with complete right hemiplegia. He was then hospitalized. The neurologic examination revealed a normal mental status without any evidence of aphasia. Cranial nerve examination was notable for right facial weakness (central type), without evidence of a Homer's Syndrome. Complete (0/5) paralysis of the right arm and leg was present. Sensation was fully intact in all 4 limbs and the face. General medical examination was unremarkable. Diffusion-weighted magnetic resonance imaging showed a large crescent-like defect in the distribution of the left MCA deep border zone area. Magnetic resonance angiography showed a normal left common carotid artery (CCA). Marked abnormal narrowing of the left cervical internal carotid artery (ICA) was observed just beyond the left CCA bifurcation (Fig I). Minimal intracranial flow was seen in the precavernous, cavernous, and supraclinoid left ICA. Both anterior carotid arteries (ACAs) had normal blood flow; the right ICA via the anterior communicating artery supplied the left ACA. Extremely scant blood flow was noted in the left MCA distribution. The study was felt to represent dissection with clot formation. Chest radiograph showed a fracture of the proximal one-third of the sternum. Plain films and computed tomography of the C Spine
373
showed degenerative changes without soft tissue swelling, fracture, or dislocation. Laboratory studies were unremarkable. Treatment with heparin was initiated. He remained hospitalized for 13 days with no change in clinical status. Repeat magnetic resonance angiography studies failed to show lysis of the left ICA clot. He then began a gradual improvement, 6 weeks after the accident he was ambulating with a cane and able to raise his right arm to shoulder level. Carotid artery dissection as a direct result of airbag deployment has been reported in children. We found only 2 adult reports. The first case,~ a 39-year-old Irish man, presented with left hemiplegia and right parietal lobe stroke immediately after a MVA. Angiography revealed bilateral ICA dissection and previously undiagnosed fibromuscular dysplasia that was felt to be a predisposing condition. He improved with systemic heparinization. The second case, 2 a 44-year-old Australian woman, was neurologically intact on arrival in the ED but 40 minutes later developed a dense right hemiplegia and aphasia secondary to left ICA dissection. The risk factors for airbag injury include short stature, small body habitus, and positioning near the steering wheel. Previously reported neurologic air bag injuries include: 1. Fatal basilar skull fracture in a short forward-positioned 17-year-old girl. 3 The fracture line transected the carotid arteries bilaterally. 2. Fatal head injury 4 (adult). 3. Lethal cervical trauma with disruption of all ventral ligaments between the skull base and the first and second vertebrae, causing medullary destruction and diffuse axonal brain injury 5 (adult). 4. Cervical central spinal cord injury causing quadriplegia secondary to flexion-extension injury 6 (adult). 5. Closed head injuries v (child). This is the first North American case we are aware of carotid dissection as a direct result of airbag deployment. This case is unusual for several reasons. The patient was an averaged sized man with no known predisposing vascular abnormalities. The onset of the neurologic symptoms was delayed approximately 24 hours, with progression over 3 days. The initial symptoms masqueraded as cervical radiculopathy, unfortunately delaying diagnosis and treatment. MALCOLM GOTTESMAN,MD
Division of Neurology BRUCE SANDEROV,MD
Department of Emergency Medicine ORLANDOORTlZ, MD
Department of Radiology Winthrop University Hospital Mineola, NY
References
FIGURE 1. Dissection of the left cervical ICA with clot formation. The right ICA supplied both ACAs, scant MCA flow was present, most likely from collateral vessels.
1. Duncan MA, Dowd N, Rawluk D, et al: Traumatic bilateral internal carotid artery dissection following airbag deployment in a patient with fibromuscular dysplasia. Br J Anaesth 2000;85:476-8 2. Thomson BN, Davis SM: Carotid artery dissection: Another airbag injury. ANZ J Surg 2001 ;71:552-553 3. Perez J, Palmatier T: Air bag-related fatality in a short, forwardpositioned driver. Ann Emerg Med December 1996;28:722-724 4. Cunningham K, Brown TD, Gradwell E, et al: Airbag associated fatal head injury: case report and review of the literature on airbag injuries. J Accid Emerg Med 2000;17-139-42 5. Hart RA, Mayberry JC, Herzberg AM: Acute cervical spinal cord injury secondary to air bag deployment without proper use of lap or shoulder harnesses. J Spinal Disord 2000;13:36-8 6. Maxeiner H, Hahn M: Airbag-induced lethal cervical trauma. J Trauma 1997;42:1148-51
374
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 20, Number 4 • July 2002
7. Marshall KW, Koch BL, Egelhoff JC: Air bag-related deaths and serious injuries in children: injury patterns and imaging findings. Am J Neuroradiol 1998; 19:1599-607
SHOULD INTRAVENOUS CONTRAST BE USED IN PATIENTS RECEIVING METFORMIN To the Editor:--Daily practice for prescribing oral agents in medical treatment of adult-onset diabetes mellitus 1 typically fails to consider a practical issue which I believe necessary for consideration in emergency medicine practice. The issue is whether to use intravenous contrast agents in patients receiving metformin. In almost every hospital in this c0untry--including small community hospitals--radiologists refuse to use intravenous contrast in such diabetic patients, even in emergency situations. I believe that the following points should be considered in any review of medical treatment for Type 2, adult-onset diabetes mellitus.
1. The rate of lactic acidosis in diabetic patients who did not receive metformin was equivalent to the rate of lactic acidosis in diabetic patients receiving metformin, a This finding suggests both that metformin may not be a cause of increased lactic acidosis and that other conditions may be causing lactic acidosis in diabetic patients. However, this retrospective study merits further investigation. Nonetheless, according to the U.S. Food and Drug Administration (FDA), lactic acidosis in patients using mefformin is rare, occurring at a rate of 5 cases per 100,000 persons. 2 2. In nonurgent situations and when serum creatinine level is within nOlTnal range (<1.5 mg/dL; < 132.6 /xmolfL), intravenous contrast agents are not contraindicated. The previously recommended step of withholding administration of metformin for 48 hours before and after administration of the intravenous contrast agent is not necessary. The same strategy applies to emergency situations in which serum creatinine level is normal. Patients in such cases should be well hydrated before receiving the intravenous contrast agent. 3,4,5 3. In nonurgent cases when the patient is receiving metformin and has a creatinine level >1.5 mg/dL (>132.6 /xmol/L), metformin administration should be replaced by alternative diabetic control (eg, insulin) for a few days before the intravenous contrast study is done. 3,4,5 4. In urgent cases when the patient has a creatinine level > 1.5 mg/dL (>132.6 /xmol/L), metformin administration should be stopped, and steps (eg, intravenous hydration) should be taken to improve renal function. The intravenous contrast study should then be done but must be accompanied by close postprocedure monitoring and alternative diabetic control.3,4,5 I hope these points will be of interest both to general and to emergency practitioners and will be helpful. The author acknowledges the Medical Editing Department, Kaiser Foundation Research Institute, for providing editorial assistance.
RAJESHGUFrA,MD Department of Emergency Medicine Kaiser Permanente Medical Center Fresno, CA
References 1. Harrigan RA, Nathan MS, Beattie P: Oral agents for the treatment of type 2 diabetes mellitus: pharmacology, toxicity, and treatment. Ann Emerg Med 2001;38:68-78
Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0025535.00/0 doi:l 0.1053/ajem.2002.33953
2. Brown JB, Pedula K, Barzilay J, et al: Lactic acidosis rates in type 2 diabetes [published erratum appears in Diabetes Care 1998; 21:2203]. Diabetes Care 1998;21:1659-63 3. Nawaz S, Cleveland T, Gaines PA, et al: Clinical risk associated with contrast angiography in metformin treated patients: a clinical review. Clin Radiol 1998;53:342-4 4. McCartney MM, Gilbert FJ, Murchison LE, et al: Metformin and contrast media--a dangerous combination? Clin Radiol 1999;54: 29-33 5. Bush WA, Bettmann MA: Metformin (Glucophage) therapy and the risk of lactic acidosis. ACR Bull 1997;53:18-9
MASSIVE HEMOPTYSIS AND HEMOTHORAX CAUSED BY PLEUROPULMONARY ANGIOSARCOMA To the Editor:--Angiosarcoma involving the lung is a rare disorder and it is usually a metastatic disease. We reported a case of pleuropulmonary epithelioid angiosarcoma in a 36-year-old woman presenting simultaneously massive hemoptysis and hemothorax and rapidly radiographic change. The presentation was rarely entertained because of its infrequency and some differences compared with that of previously reported pulmonary angiosarcoma. A 36-year-old woman presented to ED because of intermittent hemoptysis for 2 months. Body weight loss and poor appetite were also complained. Bronchoscopy and brushing smear showed negative result at outside hospital 2 weeks ago. In the ED chest radiograph (Fig 1A) showed rfiild infiltrates in right upper lung field. Bronchoscopy showed some fresh blood in right main bronchus. Brushing and washing study showed no definite result. Unfortunately, progressive dyspnea and aggravated hemoptysis developed after admission. A series of chest radiographs also showed deterioration with progressive bilateral massive pleural effusion and opacity in both lungs (Fig 1B). Echo-guided thoracentesis showed hemothorax, but effusion study and pleural biopsy revealed no definite results. Subsequent high-resolution computed tomography of chest showed multiple focal consolidated patches in both lungs, small ill-defined nodules in bilateral upper lobes, and bilateral pleural effusion. Lung perfusion scan showed low probability of pulmonary embolism. Pulmonary artery angiogram showed no embolus or tumor in pulmonary trunk and their branches. The negative antinuclear antibody and rheumatoid factor, and rheumatological consultation did not favor vasculitis. The dyspnea and hemoptysis did not improve despite of steroid, antibiotics, anti-TB agents, oxygen therapy, and effusion drainage. The final diagnosis was obtained by video-assisted thoracoscopic surgery. The operative findings showed hematoma and fibrin coating on diaphragmatic surface, and no obvious diffuse pleural thickness or mass found. Decortication of left pleura, wedge resection of lingular lobe, pleural biopsy, and left lower lobe lung biopsy, were performed. The histology of pleural and lung biopsy showed epithelioid angiosarcoma. The immunohistochemical studies showed positive for the keratin marker CAM, the endothelial markers CD31, CD34 and factor VIII, and the aggressive clinical course markers P53 and Ki67. Cardiac echo, abdominal echo, and gynecologic echo were performed and did not show any tumor. After the diagnosis was made, she received chemotherapy and died of respiratory failure within 1 month. Epithelioid angiosarcoma of respiratory system is rare and needs to exclude metastasis. Thus far, 31 cases of pleural origin, 1 1 case of tracheal origin,2 1 case of pulmonary artery origin, 3 and 1 of
Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0026535.00/0 doi:10.1053/ajem.2002.34198