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Cardiac contusion diagnosed by cardiac troponin
382
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 20, Number 4 • July 2002
thrombosis, deep vein thrombosis in lower limbs, mesenteric venous thrombosis, and pulmonary embolism. 1 In addition, several cases of involved cerebral arteries presenting hemorrhagic infarction have been reported. 2 There is no report of thalamic hemorrhage in protein C deficiency such as our case. Abdominal pain at admission suggests mesenteric venous thrombosis. The patient seemed to be in the hypercoagulable state. Although blood pressure was normal, thalamic hemorrhage occurred. There have been a few reports of hemorrhage in the basal ganglia caused by cerebral venous thrombosis in protein C deficiency. 3,4 We believe that this hemorrhagic accident was caused deep cerebral venous thrombosis in the condition of hypercoagularity. It is speculated that rhabdomyolysis may be caused by venous thrombosis in the lower legs. Protein C deficiency should be considered if a neurological accident is associated with systemic thromboembolic symptoms, even though the cerebral lesion is hemorrhagic. TAKESHIMATSUYAMA,MD
KAZUOOKUCHI,MD KE1J1 NOGAMt,MD
Department of Emergency and Critical Care Medicine
AKIRAYOSHIOKA,MD Department of Pediatrics Nara Medical University Nara; Japan
References
FIGURE 1. CT on admission showing a left thalamic hemorrhage extending to the midbrain.
patient presented with macrohematuria and fever. Laboratory data showed elevated creatine phosphokinase (2448 IU/L) and elevated myoglobin (707 ng/mL) in the serum. Urinary analysis disclosed myoglobulinemia suggesting rahbdomyolysis. Further investigations for coagulation disorders were performed to detect the cause of serial episodes. The protein C antigen level was 49% and protein C activity was 41%. These findings suggested heterozygous protein C deficiency type 1. Magnetic resonance imaging was performed to detect cerebral sinus thrombosis as one of several manifestations of coagulopathy caused by protein C deficiency. Only thalamic hemon'hage was recognized but no other abnormal vascular findings were obtained. One month later, the patient was discharged with residual neurological deficits and medicated with warfarin at the outpatient department. The hypercoagulopathy study was continued, confirming the presence of protein C deficiency. Family investigation disclosed slight decreased antigen level and activity of protein C in his father and his elder son. Protein C is a vitamin K-dependent zymogen of a plasma serine protease. It is synthesized in the liver with a molecular weight of 62 K Da. After it is activated by thrombin bound to thrombomodulin on the endothelial surface, it inhibits blood coagulation by inactivating factors Va and VIIIa. The hereditary type of protein C deficiency is transmitted as an autosomal dominant pattern. There are 2 types of deficiency. In type 1, both concentration and functional activity reduce. In type 2, concentration is normal and functional activity reduces. This deficiency leads to a hypercoagulable state in the body. Heterozygous protein C deficiency has an increased risk of thrombotic disease. Venous thrombosis is the most common clinical manifestation including cerebral venous
1. pugliese D, Nicoletti G, Andreula C, et al: Combined protein C deficiency and protein C activated resistance as a cause of caval, peripheral, and cerebral venous thrombosis--a case report. Angiology 1998;49:399-401 2. Wintzen AR, Broekmans AW, Bertina RM, et al: Cerebral haemorrhagic infarction in young patients with hereditary protein C deficiency: evidence for "spontaneous" cerebral venous thrombosis. Br Med J (Clin Res Ed) t985;290:350-352 3. Voutsinas L, Gorey MT, Gould R, et al: Venous sinus thrombosis as a cause of parenchymal and intraventricular hemorrhage in the full-term neonate. Clin Imaging 1991 ;15:273-275 4. Tarras S, Gadia C, Meister L, et al: Homozygous protein C deficiency in a newborn. Clinicopathologic correlation. Arch Neurol 1988;45:214-216
CARDIAC CONTUSION DIAGNOSED BY CARDIAC TROPONIN To the Editor:--In the setting of a severely injured trauma patient, making the diagnosis of cardiac contusion can be a difficult. Diagnosis is usually based on electrocardiogram (ECG) or echocardiographic findings. Patterns of ECG suggestive of cardiac contusion include: severe rhythm abnormalities, (multiple premature ventricular complexes, paroxysmal supraventricular tachycardia, ventricular tachycardia, and atrial or ventricular fibrillation) and severe conduction defects (second or third degree AV block, and complete bundle branch block). Echocardiographic signs include, pericardial effusion, regional wall motion abnormality, and acute valvular dysfunction. 1 However, there is not a consistent, reliable marker to aid in the diagnosis of cardiac contusion. Even cardiac troponin, which has a greater specificity than other biological markers, has a low sensitivity and low predictive values in diagnosing myocardial contusion. 2 A 25-year-old man presented to the ED after a high-speed motor vehicle collision with a tree. The patient was an unrestrained, front seat passenger in an automobile that careened off the road. The patient became pinned to the car by a large tree branch lodged
Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0032535.00/0 doi: 10.1053/ajem .2002.33958
• CORRESPONDENCE
against his chest. A prolonged extraction was required to remove the patient from the motor vehicle. On arrival in the ED, the patient was awake and alert with Glasgow Coma Scale of 15/15, complaining of pain in his chest and left arm. Vital signs were a pulse of 108 beats/min, blood pressure of 163/78 mm Hg and respiratory rate of 24 breaths/rain. On physical examination, lung sounds were clear and equal bilaterally with symmetrical chest rise and fall. No cardiac abnormalities were noted, and several abrasions were seen on the anterior chest wall. The abdomen was soft, and nontender. The left forearm had significant deformity, several skin abrasions, and no evidence of neurovascular compromise. Pulses were strong and equal in all 4 extremities. No penetrating injuries were noted. Serial ED ultrasounds showed no free fluid in the abdomen. ECG showed sinus tachycardia without ST segment change or axis deviation. Laboratory data were significant for a troponin of 7.9 ng/dL, with a peak at 10.8 ng/dL 3 hours later. Serial hematocrits were stable at 16.2 mg. Computed tomography (CT) scan of the chest showed: (1) bilateral lung contusion, (2) small bilateral pneumothoracies, (3) fracture of the right third rib, (4) perivascular soft tissue density, residual thymic tissue versus hematoma, and (5) retrosternal hematoma. The patient was admitted to the surgical team with a diagnosis of cardiac contusion. An echocardiogram, performed after transfer, showed severe aortic insufficiency with left cusp dysfunction/flail, normal left ventricular function and ejection fraction. Repair of the aortic valve was delayed to allow resolution of pulmonary contusions. The troponin fell to <0.1 ng/dL 10 days after presentation. Repair of the aortic valve occurred 14 days after presentation. Exploration of the pericardium revealed a large, posterolateral pericardial rent, with herniation of the heart into the posterior chest. Both the aortic valve, and pericardium were repaired without further complications. The patient was discharged in stable condition 4 days later. This patient was diagnosed with a cardiac contusion solely on the basis of elevated troponin, without supporting findings on ECG or echocardiogram. Given the unreliability of elevated troponin, and the necessity of ruling out other abnormalities; obtaining an echocardiogram on a patient with blunt chest trauma should be a high .priority. In addition to obtaining the appropriate studies, a thorough examination can provide valuable diagnostic clues. An aortic flail valve, causing severe aortic insufficiency, presents with a characteristic, loud, holosystolic murmur. Every clinician who examined this patient before the echocardiogram documented normal heart sounds. Examinations after the echocardiogram universally noted a III/VI holosystolic murmur. Unlike an aortic flail valve, diagnosing pericardial rent with luxation of the heart is difficult. Although some helpful clues can be found on examination, chest radiograph, ECG, and rarely, on CT, the most important factor remains a high index of suspicion. In 1864 a characteristic murmnr was reported by Morel-Lavallee. The murmur, described as sounding like a splashing mill wheel and termed "bruit de moulin," is thought to be the result of a hemopneumopericardium after pericardial rupture. 3 Although well described and discussed in the literature, this murmur is not reported in most case series. A chest radiograph may be one of the best screening tests for diagnosing pericardial tears. 4 Suggestive findings include pneumopericaridum, and displacement of the heart, s Electrocardiography may be helpful in cases of cardiac herniation, showing axis deviation toward the site of herniation. 6 CT can show cardiac malposition within the mediastinum and left chest, but is not reliable, v In this case, the best clue was the injury mechanism of injury. A significant amount of force is required to rupture the aortic valve causing aortic flail. This fact should raise suspicion of other injuries, even in the face of a stable patient. Fortunately, this
383
patient did exceedingly well despite his injuries, surviving for 2 weeks with complete luxation of the heart, a condition with a 42% survival rate. 8 AIMEE MOULIN MARK BASON-MITCHELL,MD SEAN O. HENDERSON,MD
Department of Emergency Medicine Keck School of Medicine University of Southern California Los Angeles, CA
References 1. Ferjani M, Droc G, Dreux S, et al: Circulating cardiac troponin T in myocardial contusion. Chest 1997;111:427-433 2. Bertinchant JP, Polge A, Mohty D, et al: Evaluation of incidence, clinical significance, and prognostic value of circulating cardiac troponin I and T elevation in hemodynamically stable patients with suspected myocardial contusion after blunt chest trauma. J Trauma 2000;48:924-931 3. MoreI-Lavallee: Rupture de pericarde; bruit de roue hydraulique; bruit de moulin. Gaz Med Paris 1864;19:695-696, 729730, 771-772, 803-808 4. Fulda G, Brathwaite CEM, Rodriguez A: Blunt traumatic rupture of the heart and pericardium: a ten-year experience. J Trauma 1991 ;31:167-173 5. Aho AJ, Vanttinen EA, Nelimarkka O1: Rupture of the pericardium with luxation of the heart after blunt trauma. J Trauma 1987; 27:560-563 6. Cavanaugh DG, Paris J: Pericardial rupture with complete luxation of the heart. Military Med 1983;148:28-29 7. Place RJ, Cavanaugh DG: Computed tomography to diagnose pericardial rupture. J Trauma 1995;38:822-823 8. Watkins BM, Buckley DC, Peschiera JL: Delayed presentation of pericaridal rupture with luxation of the heart following blunt trauma: a case report. J Trauma 1995;38:368-369
ULTRAVIOLET DYE MASQUERADINGAS CORNEAL ABRASION To the Editor:--Pepper spray containing oleoresin capiscum is used as a nonlethal deterrent and is associated with corneal abrasions in 7% to 9% of ED patients with ocular exposure. ~,2 Fluorescein staining and Wood's lamp or slit lamp biomicroscopic examination has been recommended for patients with ocular exposure to pepper spray. 2 We recently encountered an individual without corneal epithelial defects with fluorescence on examination caused by the ultraviolet marking dye in the pepper spray product. A 16-year-old Hispanic boy was subdued by a Dallas police officer with Punch II Streamer pepper spray (Aerko International, Ft. Landerdale, FL). The spray consists of 5% oleoresin capsicum mixed with a blend of industrial solvents used to project a coherent stream for 10 feet and an ultraviolet marking dye, Blankophor SOL (Mobay Corporation, Pittsburgh, PA). The dye is a benzo pyranone optical brightener that is visible under a black light and cannot be washed off for at least 24 hours. The subject was handcuffed and brought to the Parkland Memorial Hospital ED complaining of right eye irritation and redness. Ophthalmology was consulted when diffuse corneal staining was detected after instillation of 0.25% fluorescein dye. Visual acuity was 20/20 in each eye, and slit lamp biomicroscopy revealed intact corneal epithelium without corneal infiltrates in each eye. However, there was diffuse fluorescence of the cornea and conjunctival epithelium in each eye
Supported in part by an unrestricted research grant from Research to Prevent Blindness, Inc., New York, NY. Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0033535.00/0 doi: 10.1053/ajem.2002.33954
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 20, Number 4 • July 2002
thrombosis, deep vein thrombosis in lower limbs, mesenteric venous thrombosis, and pulmonary embolism. 1 In addition, several cases of involved cerebral arteries presenting hemorrhagic infarction have been reported. 2 There is no report of thalamic hemorrhage in protein C deficiency such as our case. Abdominal pain at admission suggests mesenteric venous thrombosis. The patient seemed to be in the hypercoagulable state. Although blood pressure was normal, thalamic hemorrhage occurred. There have been a few reports of hemorrhage in the basal ganglia caused by cerebral venous thrombosis in protein C deficiency. 3,4 We believe that this hemorrhagic accident was caused deep cerebral venous thrombosis in the condition of hypercoagularity. It is speculated that rhabdomyolysis may be caused by venous thrombosis in the lower legs. Protein C deficiency should be considered if a neurological accident is associated with systemic thromboembolic symptoms, even though the cerebral lesion is hemorrhagic. TAKESHIMATSUYAMA,MD
KAZUOOKUCHI,MD KE1J1 NOGAMt,MD
Department of Emergency and Critical Care Medicine
AKIRAYOSHIOKA,MD Department of Pediatrics Nara Medical University Nara; Japan
References
FIGURE 1. CT on admission showing a left thalamic hemorrhage extending to the midbrain.
patient presented with macrohematuria and fever. Laboratory data showed elevated creatine phosphokinase (2448 IU/L) and elevated myoglobin (707 ng/mL) in the serum. Urinary analysis disclosed myoglobulinemia suggesting rahbdomyolysis. Further investigations for coagulation disorders were performed to detect the cause of serial episodes. The protein C antigen level was 49% and protein C activity was 41%. These findings suggested heterozygous protein C deficiency type 1. Magnetic resonance imaging was performed to detect cerebral sinus thrombosis as one of several manifestations of coagulopathy caused by protein C deficiency. Only thalamic hemon'hage was recognized but no other abnormal vascular findings were obtained. One month later, the patient was discharged with residual neurological deficits and medicated with warfarin at the outpatient department. The hypercoagulopathy study was continued, confirming the presence of protein C deficiency. Family investigation disclosed slight decreased antigen level and activity of protein C in his father and his elder son. Protein C is a vitamin K-dependent zymogen of a plasma serine protease. It is synthesized in the liver with a molecular weight of 62 K Da. After it is activated by thrombin bound to thrombomodulin on the endothelial surface, it inhibits blood coagulation by inactivating factors Va and VIIIa. The hereditary type of protein C deficiency is transmitted as an autosomal dominant pattern. There are 2 types of deficiency. In type 1, both concentration and functional activity reduce. In type 2, concentration is normal and functional activity reduces. This deficiency leads to a hypercoagulable state in the body. Heterozygous protein C deficiency has an increased risk of thrombotic disease. Venous thrombosis is the most common clinical manifestation including cerebral venous
1. pugliese D, Nicoletti G, Andreula C, et al: Combined protein C deficiency and protein C activated resistance as a cause of caval, peripheral, and cerebral venous thrombosis--a case report. Angiology 1998;49:399-401 2. Wintzen AR, Broekmans AW, Bertina RM, et al: Cerebral haemorrhagic infarction in young patients with hereditary protein C deficiency: evidence for "spontaneous" cerebral venous thrombosis. Br Med J (Clin Res Ed) t985;290:350-352 3. Voutsinas L, Gorey MT, Gould R, et al: Venous sinus thrombosis as a cause of parenchymal and intraventricular hemorrhage in the full-term neonate. Clin Imaging 1991 ;15:273-275 4. Tarras S, Gadia C, Meister L, et al: Homozygous protein C deficiency in a newborn. Clinicopathologic correlation. Arch Neurol 1988;45:214-216
CARDIAC CONTUSION DIAGNOSED BY CARDIAC TROPONIN To the Editor:--In the setting of a severely injured trauma patient, making the diagnosis of cardiac contusion can be a difficult. Diagnosis is usually based on electrocardiogram (ECG) or echocardiographic findings. Patterns of ECG suggestive of cardiac contusion include: severe rhythm abnormalities, (multiple premature ventricular complexes, paroxysmal supraventricular tachycardia, ventricular tachycardia, and atrial or ventricular fibrillation) and severe conduction defects (second or third degree AV block, and complete bundle branch block). Echocardiographic signs include, pericardial effusion, regional wall motion abnormality, and acute valvular dysfunction. 1 However, there is not a consistent, reliable marker to aid in the diagnosis of cardiac contusion. Even cardiac troponin, which has a greater specificity than other biological markers, has a low sensitivity and low predictive values in diagnosing myocardial contusion. 2 A 25-year-old man presented to the ED after a high-speed motor vehicle collision with a tree. The patient was an unrestrained, front seat passenger in an automobile that careened off the road. The patient became pinned to the car by a large tree branch lodged
Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0032535.00/0 doi: 10.1053/ajem .2002.33958
• CORRESPONDENCE
against his chest. A prolonged extraction was required to remove the patient from the motor vehicle. On arrival in the ED, the patient was awake and alert with Glasgow Coma Scale of 15/15, complaining of pain in his chest and left arm. Vital signs were a pulse of 108 beats/min, blood pressure of 163/78 mm Hg and respiratory rate of 24 breaths/rain. On physical examination, lung sounds were clear and equal bilaterally with symmetrical chest rise and fall. No cardiac abnormalities were noted, and several abrasions were seen on the anterior chest wall. The abdomen was soft, and nontender. The left forearm had significant deformity, several skin abrasions, and no evidence of neurovascular compromise. Pulses were strong and equal in all 4 extremities. No penetrating injuries were noted. Serial ED ultrasounds showed no free fluid in the abdomen. ECG showed sinus tachycardia without ST segment change or axis deviation. Laboratory data were significant for a troponin of 7.9 ng/dL, with a peak at 10.8 ng/dL 3 hours later. Serial hematocrits were stable at 16.2 mg. Computed tomography (CT) scan of the chest showed: (1) bilateral lung contusion, (2) small bilateral pneumothoracies, (3) fracture of the right third rib, (4) perivascular soft tissue density, residual thymic tissue versus hematoma, and (5) retrosternal hematoma. The patient was admitted to the surgical team with a diagnosis of cardiac contusion. An echocardiogram, performed after transfer, showed severe aortic insufficiency with left cusp dysfunction/flail, normal left ventricular function and ejection fraction. Repair of the aortic valve was delayed to allow resolution of pulmonary contusions. The troponin fell to <0.1 ng/dL 10 days after presentation. Repair of the aortic valve occurred 14 days after presentation. Exploration of the pericardium revealed a large, posterolateral pericardial rent, with herniation of the heart into the posterior chest. Both the aortic valve, and pericardium were repaired without further complications. The patient was discharged in stable condition 4 days later. This patient was diagnosed with a cardiac contusion solely on the basis of elevated troponin, without supporting findings on ECG or echocardiogram. Given the unreliability of elevated troponin, and the necessity of ruling out other abnormalities; obtaining an echocardiogram on a patient with blunt chest trauma should be a high .priority. In addition to obtaining the appropriate studies, a thorough examination can provide valuable diagnostic clues. An aortic flail valve, causing severe aortic insufficiency, presents with a characteristic, loud, holosystolic murmur. Every clinician who examined this patient before the echocardiogram documented normal heart sounds. Examinations after the echocardiogram universally noted a III/VI holosystolic murmur. Unlike an aortic flail valve, diagnosing pericardial rent with luxation of the heart is difficult. Although some helpful clues can be found on examination, chest radiograph, ECG, and rarely, on CT, the most important factor remains a high index of suspicion. In 1864 a characteristic murmnr was reported by Morel-Lavallee. The murmur, described as sounding like a splashing mill wheel and termed "bruit de moulin," is thought to be the result of a hemopneumopericardium after pericardial rupture. 3 Although well described and discussed in the literature, this murmur is not reported in most case series. A chest radiograph may be one of the best screening tests for diagnosing pericardial tears. 4 Suggestive findings include pneumopericaridum, and displacement of the heart, s Electrocardiography may be helpful in cases of cardiac herniation, showing axis deviation toward the site of herniation. 6 CT can show cardiac malposition within the mediastinum and left chest, but is not reliable, v In this case, the best clue was the injury mechanism of injury. A significant amount of force is required to rupture the aortic valve causing aortic flail. This fact should raise suspicion of other injuries, even in the face of a stable patient. Fortunately, this
383
patient did exceedingly well despite his injuries, surviving for 2 weeks with complete luxation of the heart, a condition with a 42% survival rate. 8 AIMEE MOULIN MARK BASON-MITCHELL,MD SEAN O. HENDERSON,MD
Department of Emergency Medicine Keck School of Medicine University of Southern California Los Angeles, CA
References 1. Ferjani M, Droc G, Dreux S, et al: Circulating cardiac troponin T in myocardial contusion. Chest 1997;111:427-433 2. Bertinchant JP, Polge A, Mohty D, et al: Evaluation of incidence, clinical significance, and prognostic value of circulating cardiac troponin I and T elevation in hemodynamically stable patients with suspected myocardial contusion after blunt chest trauma. J Trauma 2000;48:924-931 3. MoreI-Lavallee: Rupture de pericarde; bruit de roue hydraulique; bruit de moulin. Gaz Med Paris 1864;19:695-696, 729730, 771-772, 803-808 4. Fulda G, Brathwaite CEM, Rodriguez A: Blunt traumatic rupture of the heart and pericardium: a ten-year experience. J Trauma 1991 ;31:167-173 5. Aho AJ, Vanttinen EA, Nelimarkka O1: Rupture of the pericardium with luxation of the heart after blunt trauma. J Trauma 1987; 27:560-563 6. Cavanaugh DG, Paris J: Pericardial rupture with complete luxation of the heart. Military Med 1983;148:28-29 7. Place RJ, Cavanaugh DG: Computed tomography to diagnose pericardial rupture. J Trauma 1995;38:822-823 8. Watkins BM, Buckley DC, Peschiera JL: Delayed presentation of pericaridal rupture with luxation of the heart following blunt trauma: a case report. J Trauma 1995;38:368-369
ULTRAVIOLET DYE MASQUERADINGAS CORNEAL ABRASION To the Editor:--Pepper spray containing oleoresin capiscum is used as a nonlethal deterrent and is associated with corneal abrasions in 7% to 9% of ED patients with ocular exposure. ~,2 Fluorescein staining and Wood's lamp or slit lamp biomicroscopic examination has been recommended for patients with ocular exposure to pepper spray. 2 We recently encountered an individual without corneal epithelial defects with fluorescence on examination caused by the ultraviolet marking dye in the pepper spray product. A 16-year-old Hispanic boy was subdued by a Dallas police officer with Punch II Streamer pepper spray (Aerko International, Ft. Landerdale, FL). The spray consists of 5% oleoresin capsicum mixed with a blend of industrial solvents used to project a coherent stream for 10 feet and an ultraviolet marking dye, Blankophor SOL (Mobay Corporation, Pittsburgh, PA). The dye is a benzo pyranone optical brightener that is visible under a black light and cannot be washed off for at least 24 hours. The subject was handcuffed and brought to the Parkland Memorial Hospital ED complaining of right eye irritation and redness. Ophthalmology was consulted when diffuse corneal staining was detected after instillation of 0.25% fluorescein dye. Visual acuity was 20/20 in each eye, and slit lamp biomicroscopy revealed intact corneal epithelium without corneal infiltrates in each eye. However, there was diffuse fluorescence of the cornea and conjunctival epithelium in each eye
Supported in part by an unrestricted research grant from Research to Prevent Blindness, Inc., New York, NY. Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0033535.00/0 doi: 10.1053/ajem.2002.33954