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An unusual presentation of renal infarction
CORRESPONDENCE
FIGURE 2. Abdominal CT shows the suspect of duodenal rupture caused by multiple air pocket noted at right posterior pararenal space with contrast leakage from duodenum (4). trografin, Schering, Berlin, Germany) material from the esophagus into the surrounding mediastinum, and absence of mediastinal air. Emergent video-assisted thoracoscopy surgery (VATS) was performed to provide drainage of the empyema. No bronchopleural fistula, blebs, bulla, laceration of lung, esophageal leakage, and no evidence of infection or contusion of the surrounding pulmonary parenchyma were found. The parietal and visceral layers of the pleura and the surrounding diaphragm were intact. Abdominal CT, however, showed the suspect of duodenal rupture caused by multiple air pocket noted at right posterior pararenal space with contrast leakage from duodenum (Fig 2) On laparatomy, a 0.5 ⫻ 0.5 cm2 periduodenal abscess caused by duodenal rupture and pus drainage was found, and jejunostomy was done. Klebsiella pneumoniae, Enterobacter cloacae, and Enterococcus faecalis later grew on culture of this abscess. The patient’s postoperative course was uncomplicated. A follow-up chest X-ray film showed significant clearing of both lung bases. The patient was discharged to complete a 6-week course of oral amoxicillin and clavulanate potassium. The chest X-ray film of our patient revealed hydropneumothorax. Hemopneumothorax is the usual first impression because this diagnosis is a frequent sequel of blunt chest trauma.1 Initial thoracentesis was performed and the microscopic examination of the pleural fluid was consistent with pyopneumothorax. The cause of pyopneumothorax in our patient was thought to be the presence of esophageal injury, an injury to the tracheobronchial tree with or without lung infection, or initially infected retained hemothorax.2 VATS did not find any pulmonary lesions. Because laparatomy revealed a periduodenal rupture and the presence of the gastrointestinal flora growing both from the empyema and periduodenal abscess, we believed that our patient’s empyema was attributable to spreading of bacteria from this periduodenal abscess, and the pneumothorax caused by gas formation by these bacterial pathogens. In fact, no chest or thoracic injuries were evident. Arom and associates reported a 6% incidence of empyema in 300 cases of chest trauma.3 Steps in the pathogenesis of posttraumatic empyema are as follows: (1) primary or direct contamination at time of injury, (2) secondary contamination from initial treatment of injury, (3) parapneumonic process or typical postpneumonic bacterial infection, (4) a blood drainage problem or failure preventing visceral and parietal pleural apposition, and (5) subdiaphragmatic processes may contaminate the pleural space directly by missiles or foreign bodies or indirectly through transdiaphragmatic lymphatics.3,4,5,6 In our case, the last pathogenic mechanism
437
applies in that a subdiaphragmatic infection probably led to the empyema indirectly by transdiaphragmatic lymphatic transmission of the bacteria. The presence of mixed gastrointestinal floras in thoracentesis drainage suggested the possible diagnosis of abdominal sepsis. The minimal abdominal signs and symptoms makes incrimination of the abdomen as the source of infection more difficult, and early diagnosis is dependent on a high degree of suspicion. Intra-abdominal infection as a cause of empyema has been previously described.7 Imaging of the abdomen may be necessary to identify a subdiaphragmatic source of infection, such as periduodenal abscess in our case. Abdominal CT is highly specific, sensitive, and accurate in establishing the diagnosis of periduodenal abscess.8 Elimination of the primary infected focus is paramount. In our case, treatment required administration of systemic antibiotics, and a surgical procedure to eliminate the primary infectious focus. Roentgenographic manifestation of hydropneumothorax in blunt trauma patients is frequently attributable to hemopneumothorax. Another consideration is pyopneumothorax. If no thoracic injury is found in the trauma work up, abdominal sepsis leading to secondary contamination of the pleural space, and consequently empyema, should always be considered. It should be promptly treated. Any delay or neglect of this differential diagnosis after blunt injury can lead to high morbidity and mortality. TE-I WENG, MD ANG YUAN, MD WEN-JONE CHEN, MD, PhD Department of Emergency Medicine National Taiwan University Hospital Taipei, Taiwan
References 1. Sturm JT, Points BJ, Perry JF: Hemopneumothorax following blunt trauma of the thorax. Surg Gynecol Obstet 1975;141:539-540 2. Richardson JD, Miller FB, Carrillo EH, et al: Complex thoracic injuries. Surg Clin North Am 1996;76:725-748 3. Arom KV, Grover FL, Richardson JD, et al: Posttraumatic empyema. Am Thorac Surg 1977;23:254-258 4. Richardson JD, Carrillo E: Thoracic infection after trauma. Chest Surg Clin N Am 1997;7:401-427 5. Coon JL, Shuck JM: Failure of tube thoracostomy for posttraumatic empyema: an indication for early decortication. J Trauma 1975;15:588-594 6. Beall AC Jr, Crawford HW, DeBakey ME: Considerations in the management of acute traumatic hemothorax. J Thorac Cardiovasc Surg 1966;52:351-360 7. Herline A, Burton EM, Hatley R: Thoracic empyema in a patient with acute appendicitis: a rare association. J Pediatr Surg 1994;29: 1623-1625 8. Whitley NO, Shatney CM: Diagnosis of abdominal abscesses in patients with major trauma: the use of computed tomography. Radiology 1983;147:179-183
AN UNUSUAL PRESENTATION OF RENAL INFARCTION To the Editor:—A 75-year-old woman with a prior history of atrial fibrillation, hypertension, and nephrolithiasis presented to the emergency department (ED) with a chief complaint of left lower quadrant (LLQ) pain of 16 hours duration. The patient stated the pain began suddenly at 6pm the previous night with the onset of nausea and vomiting shortly thereafter. The pain was described as a constant, aching, severe pain that continued throughout the night. It began at rest, and was without exacerbating or relieving factors. Initially the pain was nonradiating, but throughout the night some
© 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2205-0012$30.00/0 doi:10.1016/j.ajem.2004.06.003
438
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 22, Number 5 ■ September 2004
minor radiation to the left upper quadrant (LUQ) and epigastrum was noted. Nausea and vomiting continued throughout the night. On review, the patient described a mild, sharp, intermittent flank pain in 2 weeks preceding presentation. She denied hematemesis, diarrhea, change in bowel habits, dysuria, polyuria, hematuria, fevers, chills, hematochezia, melena, shortness of breath, or cough but did acknowledge a headache. Her prescriptions included Atenolol 50 mg/day orally, Cardizem 60 mg orally 4 times daily, and Coumadin 7.5 mg/day orally. On examination, vital signs were a temperature of 97.7°F, blood pressure 254/98 mmHg, pulse 80 beats/min, respiratory rate 18 breaths/min, and oxygen saturation 97%. Patient was a healthy appearing elderly woman, moderately obese, in mild/moderate distress. Mucous membranes were moist, neck was supple, and there was no jugular venous distension. Cardiovascular exam revealed regular rate and rhythm with a 2/6 systolic ejection murmur radiating into the neck. Chest was clear to auscultation bilaterally. Abdomen was soft, moderately tender to palpation. There was moderate tenderness in the upper LLQ with mild tenderness in the lower LLQ and LUQ, and minimal tenderness of the epigastrum. There was voluntary guarding at the point of maximal tenderness but no rebound. Bowel sounds were hypoactive and there was no pulsatile mass. No CVA tenderness was noted. Stool was heme negative. Laboratory data included a WBC of 15.7 without a left shift and a HgB of 15.9. Chemistry and liver function tests were within normal limits. INR was 2.5. Urinalysis demonstrated 150/uL of blood but no RBCs or WBCs, and was otherwise negative. Patient was preliminarily diagnosed with acute abdominal pain and a contrast CT scan was done which showed a complete left renal infarction. The Urology, Renal, and Hematology/Oncology services were consulted and the patient was admitted to the hospital. Workup in house showed complete obstruction of arterial flow with diffuse atherosclerosis. The LDH was elevated and increased for 2 more days to a peak of 842 and resolved. Given the atypical nature of this presentation, a hypercoagulable workup was completed and eventually returned significant for anticardiolipin antibody. Patient was discharged on Lovenox with a plan to transition back to Coumadin at a higher therapeutic dose. Renal Infarction is a very uncommon and difficult diagnosis to make, but one in which misdiagnosis can have serious repercussions. One restrospective study placed its incidence at 0.007%.1 The causes in descending order of frequency are thought to be traumatic, thromboembolic (90% from atrial fibrillation), atheroembolic, and thrombotic. Risk factors include cardiovascular disease likely to lead to thrombus formation, local surgical manipu-
lation, or systemic disease (infection, inflammation, or hypercoagulable) states. There have been a number of reports implicating cocaine in renal infarction.2,3 Clinical presentation (in the nontraumatic setting) is usually one of sudden onset flank or abdominal pain with nausea, vomiting, and fever. On exam patients are hypertensive and have local tenderness without peritoneal signs. Some patients have hematuria, and elevated CPK or AST but it is generally accepted that patients can be diagnosed based on an elevated LDH. Any number of imaging studies, including IV contrast CT, Doppler ultrasound, MRA, or arteriogram are considered diagnostic, but there are no data elucidating the sensitivities of these modalities. Management is almost always medical except in patient’s with a traumatic cause or a single kidney. This case is reported because it is atypical in many aspects and shows the difficulty of diagnosis and the necessity to be thorough in similar presentations. This was a case of an appropriately anticoagulated, rate controlled, elderly woman who presented with anterior abdominal pain; all of these features are not generally considered typical presentations in literature reviewing this disease.4 However, even the “typical” presentations can be difficult to diagnose. In fact, in a recently published retrospective study,1 11 patients diagnosed with renal infarction were all initially misdiagnosed. The most common misdiagnoses were nephrolithiasis and pyelonephritis. Many of these patients received CT scans that showed the cause, but the CT was misread. The investigators also showed a long time between symptoms and diagnosis, underscoring the potential morbidity associated with missed diagnosis. Because of the rarity of this condition, the clinician and the radiologist must remember to include renal infarction in the differential of those with undiagnosed abdominal pain and the risk factors described above. ANTHONY NAPOLI, MD Rhode Island Hospital Providence, RI
References 1. Korzets Z, Cecilia OL, Ughi G, et al: The clinical spectrum of acute renal infarction. IMAJ 2002;4:781-784 2. Sharff JA: Renal infarction associated with intravenous cocaine use. Ann Emerg Med 1984;13:1145-1147 3. Goodman PE, Rennie WP: Renal infarction secondary to nasal insufflation of cocaine. Am J Emerg Med 1995;13:421-423 4. Manfredini R, et al: Renal infarction: An uncommon mimic presenting with flank pain. Am J Emerg Med 2000;18(3):325-327
FIGURE 2. Abdominal CT shows the suspect of duodenal rupture caused by multiple air pocket noted at right posterior pararenal space with contrast leakage from duodenum (4). trografin, Schering, Berlin, Germany) material from the esophagus into the surrounding mediastinum, and absence of mediastinal air. Emergent video-assisted thoracoscopy surgery (VATS) was performed to provide drainage of the empyema. No bronchopleural fistula, blebs, bulla, laceration of lung, esophageal leakage, and no evidence of infection or contusion of the surrounding pulmonary parenchyma were found. The parietal and visceral layers of the pleura and the surrounding diaphragm were intact. Abdominal CT, however, showed the suspect of duodenal rupture caused by multiple air pocket noted at right posterior pararenal space with contrast leakage from duodenum (Fig 2) On laparatomy, a 0.5 ⫻ 0.5 cm2 periduodenal abscess caused by duodenal rupture and pus drainage was found, and jejunostomy was done. Klebsiella pneumoniae, Enterobacter cloacae, and Enterococcus faecalis later grew on culture of this abscess. The patient’s postoperative course was uncomplicated. A follow-up chest X-ray film showed significant clearing of both lung bases. The patient was discharged to complete a 6-week course of oral amoxicillin and clavulanate potassium. The chest X-ray film of our patient revealed hydropneumothorax. Hemopneumothorax is the usual first impression because this diagnosis is a frequent sequel of blunt chest trauma.1 Initial thoracentesis was performed and the microscopic examination of the pleural fluid was consistent with pyopneumothorax. The cause of pyopneumothorax in our patient was thought to be the presence of esophageal injury, an injury to the tracheobronchial tree with or without lung infection, or initially infected retained hemothorax.2 VATS did not find any pulmonary lesions. Because laparatomy revealed a periduodenal rupture and the presence of the gastrointestinal flora growing both from the empyema and periduodenal abscess, we believed that our patient’s empyema was attributable to spreading of bacteria from this periduodenal abscess, and the pneumothorax caused by gas formation by these bacterial pathogens. In fact, no chest or thoracic injuries were evident. Arom and associates reported a 6% incidence of empyema in 300 cases of chest trauma.3 Steps in the pathogenesis of posttraumatic empyema are as follows: (1) primary or direct contamination at time of injury, (2) secondary contamination from initial treatment of injury, (3) parapneumonic process or typical postpneumonic bacterial infection, (4) a blood drainage problem or failure preventing visceral and parietal pleural apposition, and (5) subdiaphragmatic processes may contaminate the pleural space directly by missiles or foreign bodies or indirectly through transdiaphragmatic lymphatics.3,4,5,6 In our case, the last pathogenic mechanism
437
applies in that a subdiaphragmatic infection probably led to the empyema indirectly by transdiaphragmatic lymphatic transmission of the bacteria. The presence of mixed gastrointestinal floras in thoracentesis drainage suggested the possible diagnosis of abdominal sepsis. The minimal abdominal signs and symptoms makes incrimination of the abdomen as the source of infection more difficult, and early diagnosis is dependent on a high degree of suspicion. Intra-abdominal infection as a cause of empyema has been previously described.7 Imaging of the abdomen may be necessary to identify a subdiaphragmatic source of infection, such as periduodenal abscess in our case. Abdominal CT is highly specific, sensitive, and accurate in establishing the diagnosis of periduodenal abscess.8 Elimination of the primary infected focus is paramount. In our case, treatment required administration of systemic antibiotics, and a surgical procedure to eliminate the primary infectious focus. Roentgenographic manifestation of hydropneumothorax in blunt trauma patients is frequently attributable to hemopneumothorax. Another consideration is pyopneumothorax. If no thoracic injury is found in the trauma work up, abdominal sepsis leading to secondary contamination of the pleural space, and consequently empyema, should always be considered. It should be promptly treated. Any delay or neglect of this differential diagnosis after blunt injury can lead to high morbidity and mortality. TE-I WENG, MD ANG YUAN, MD WEN-JONE CHEN, MD, PhD Department of Emergency Medicine National Taiwan University Hospital Taipei, Taiwan
References 1. Sturm JT, Points BJ, Perry JF: Hemopneumothorax following blunt trauma of the thorax. Surg Gynecol Obstet 1975;141:539-540 2. Richardson JD, Miller FB, Carrillo EH, et al: Complex thoracic injuries. Surg Clin North Am 1996;76:725-748 3. Arom KV, Grover FL, Richardson JD, et al: Posttraumatic empyema. Am Thorac Surg 1977;23:254-258 4. Richardson JD, Carrillo E: Thoracic infection after trauma. Chest Surg Clin N Am 1997;7:401-427 5. Coon JL, Shuck JM: Failure of tube thoracostomy for posttraumatic empyema: an indication for early decortication. J Trauma 1975;15:588-594 6. Beall AC Jr, Crawford HW, DeBakey ME: Considerations in the management of acute traumatic hemothorax. J Thorac Cardiovasc Surg 1966;52:351-360 7. Herline A, Burton EM, Hatley R: Thoracic empyema in a patient with acute appendicitis: a rare association. J Pediatr Surg 1994;29: 1623-1625 8. Whitley NO, Shatney CM: Diagnosis of abdominal abscesses in patients with major trauma: the use of computed tomography. Radiology 1983;147:179-183
AN UNUSUAL PRESENTATION OF RENAL INFARCTION To the Editor:—A 75-year-old woman with a prior history of atrial fibrillation, hypertension, and nephrolithiasis presented to the emergency department (ED) with a chief complaint of left lower quadrant (LLQ) pain of 16 hours duration. The patient stated the pain began suddenly at 6pm the previous night with the onset of nausea and vomiting shortly thereafter. The pain was described as a constant, aching, severe pain that continued throughout the night. It began at rest, and was without exacerbating or relieving factors. Initially the pain was nonradiating, but throughout the night some
© 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2205-0012$30.00/0 doi:10.1016/j.ajem.2004.06.003
438
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 22, Number 5 ■ September 2004
minor radiation to the left upper quadrant (LUQ) and epigastrum was noted. Nausea and vomiting continued throughout the night. On review, the patient described a mild, sharp, intermittent flank pain in 2 weeks preceding presentation. She denied hematemesis, diarrhea, change in bowel habits, dysuria, polyuria, hematuria, fevers, chills, hematochezia, melena, shortness of breath, or cough but did acknowledge a headache. Her prescriptions included Atenolol 50 mg/day orally, Cardizem 60 mg orally 4 times daily, and Coumadin 7.5 mg/day orally. On examination, vital signs were a temperature of 97.7°F, blood pressure 254/98 mmHg, pulse 80 beats/min, respiratory rate 18 breaths/min, and oxygen saturation 97%. Patient was a healthy appearing elderly woman, moderately obese, in mild/moderate distress. Mucous membranes were moist, neck was supple, and there was no jugular venous distension. Cardiovascular exam revealed regular rate and rhythm with a 2/6 systolic ejection murmur radiating into the neck. Chest was clear to auscultation bilaterally. Abdomen was soft, moderately tender to palpation. There was moderate tenderness in the upper LLQ with mild tenderness in the lower LLQ and LUQ, and minimal tenderness of the epigastrum. There was voluntary guarding at the point of maximal tenderness but no rebound. Bowel sounds were hypoactive and there was no pulsatile mass. No CVA tenderness was noted. Stool was heme negative. Laboratory data included a WBC of 15.7 without a left shift and a HgB of 15.9. Chemistry and liver function tests were within normal limits. INR was 2.5. Urinalysis demonstrated 150/uL of blood but no RBCs or WBCs, and was otherwise negative. Patient was preliminarily diagnosed with acute abdominal pain and a contrast CT scan was done which showed a complete left renal infarction. The Urology, Renal, and Hematology/Oncology services were consulted and the patient was admitted to the hospital. Workup in house showed complete obstruction of arterial flow with diffuse atherosclerosis. The LDH was elevated and increased for 2 more days to a peak of 842 and resolved. Given the atypical nature of this presentation, a hypercoagulable workup was completed and eventually returned significant for anticardiolipin antibody. Patient was discharged on Lovenox with a plan to transition back to Coumadin at a higher therapeutic dose. Renal Infarction is a very uncommon and difficult diagnosis to make, but one in which misdiagnosis can have serious repercussions. One restrospective study placed its incidence at 0.007%.1 The causes in descending order of frequency are thought to be traumatic, thromboembolic (90% from atrial fibrillation), atheroembolic, and thrombotic. Risk factors include cardiovascular disease likely to lead to thrombus formation, local surgical manipu-
lation, or systemic disease (infection, inflammation, or hypercoagulable) states. There have been a number of reports implicating cocaine in renal infarction.2,3 Clinical presentation (in the nontraumatic setting) is usually one of sudden onset flank or abdominal pain with nausea, vomiting, and fever. On exam patients are hypertensive and have local tenderness without peritoneal signs. Some patients have hematuria, and elevated CPK or AST but it is generally accepted that patients can be diagnosed based on an elevated LDH. Any number of imaging studies, including IV contrast CT, Doppler ultrasound, MRA, or arteriogram are considered diagnostic, but there are no data elucidating the sensitivities of these modalities. Management is almost always medical except in patient’s with a traumatic cause or a single kidney. This case is reported because it is atypical in many aspects and shows the difficulty of diagnosis and the necessity to be thorough in similar presentations. This was a case of an appropriately anticoagulated, rate controlled, elderly woman who presented with anterior abdominal pain; all of these features are not generally considered typical presentations in literature reviewing this disease.4 However, even the “typical” presentations can be difficult to diagnose. In fact, in a recently published retrospective study,1 11 patients diagnosed with renal infarction were all initially misdiagnosed. The most common misdiagnoses were nephrolithiasis and pyelonephritis. Many of these patients received CT scans that showed the cause, but the CT was misread. The investigators also showed a long time between symptoms and diagnosis, underscoring the potential morbidity associated with missed diagnosis. Because of the rarity of this condition, the clinician and the radiologist must remember to include renal infarction in the differential of those with undiagnosed abdominal pain and the risk factors described above. ANTHONY NAPOLI, MD Rhode Island Hospital Providence, RI
References 1. Korzets Z, Cecilia OL, Ughi G, et al: The clinical spectrum of acute renal infarction. IMAJ 2002;4:781-784 2. Sharff JA: Renal infarction associated with intravenous cocaine use. Ann Emerg Med 1984;13:1145-1147 3. Goodman PE, Rennie WP: Renal infarction secondary to nasal insufflation of cocaine. Am J Emerg Med 1995;13:421-423 4. Manfredini R, et al: Renal infarction: An uncommon mimic presenting with flank pain. Am J Emerg Med 2000;18(3):325-327