260
Brief Communications
American
January IS92 Heart Journal
fractionation during stimulations (Fig. 3). (4) The notch, which showed a bradycardia-dependent exaggeration, also characterizes the ECG of this patient and might be closely related to the arrhythmogenic substrate, as suggested from the change observed after the ablation procedure (Fig. 1, A and B). The outcome of an attempt at catheter ablation was excellent, and the patient is waiting for a reevaluation examination. Furthermore, use of the AICD will now be indicated. REFERENCES 1. Mmorwski
M, Reide
PR, Mower
MM,
et al. Termination
malignant ventricular arrhythmias with implantable lator in human beings. N Enel 2. Josephson ME, Horowitz LN, Greenspan AM. Role of catheter
evaluation
of ventricular
of
defibril-
J Med 1980:303:322-4. Spielman SR, Waxman HL, mapping in the preoperative
tachycsrdia.
Am J Cardiol 1982;
49207-20. 3. Aizawa Y, Satou M, Funaxaki T, Aiiawa M, Suzuki K, Shibata A, Josephson ME. Early experiences of endocardial catheter mapping of the left ventricle in sustained ventricular tachy-
cardia. Efficacy, safety and complication. 51:1283-g 4. Niwano
S, Aizawa
Y, Satoh
M, Shibata
Jpn Circ J 1987;
A. Low energy
electri-
cal catheter ablation of sustained ventricular tachycardia originating from the right ventricle. AM HEART J 1989; 117:1155-7. 5. Benson
DW,
Benditt
DG, Anderson
RW,
et al. Cardiac
arrest
in young, ostensibly healthy patients: clinical, hemodynsmic, and electrophysiologic findings. Am J Cardiol 198%52:65-g. 6. Belhassen B, Shapga I, Schoshani D, Paredes A, Miller H, Laniado S. Idiopathic ventricular fibrillation: inducibility and beneficial effects of class I antiarrhythmic agents. Circulation
1987;75:899-16.
Tricuspid atresia associated with aortopulmonary window: Controlling pulmonary blood flow with a fenestrated patch Tal Geva, MD,* David A. Ott, MD,b Achi Ludomirsky, MD,a Susan J. Argyle, MD, and Martin P. O’Laughlin, MD.” Houston, Texas
Aortopulmonary (AP) window is an uncommon anomaly, with an incidence of less than one per 1000 cases of congenital heart disease. l-3 The defect, first reported in 1820,4 is associated with other cardiovascular malformations in one third to one half of cases. The most frequent
From *the Lillie Frank Abercrombie Section of Pediatric Cardiology, Department of Pediatrics, Baylor College of Medicine and Texas Children’s Hospital; and bthe Department of Thoracic and Cardiovascular Surgery, St Luke’s Episcopal Hospital, Texas Children’s Hospital, Texas Heart Institute. Reprint Hospital,
requests: Houston,
4/4/33327
Tal Geva, MD, TX 77030.
Pediatric
Cardiology,
Texas
Children’s
Fig. 1. Two-dimensional echocardiogram from the high left parasternal short-axis view showing the ascending aorta (AO), main pulmonary artery (MPA), and its bifurcation. The large aortopulmonary window (arrow) involves the proximal segments of the great arteries.
association has been with patent ductus arteriosus, followed by ventricular septal defect, tetralogy of Fallot, subaortic stenosis, coarctation of the aorta, interrupted aortic arch, anomalous origin of the right or left coronary artery from the pulmonary artery, anomalous origin of the right pulmonary artery from the aorta, and bicuspid aortic valve.3 The coexistence of an AP window with tricuspid atresia has not previously been documented. We report a case of tricuspid atresia with an AP window. Since the infant had tricuspid atresia with subvalvar and valvar pulmonary stenosis, she required augmented pulmonary blood flow; rather than closing the AP window and creating a new systemic-to-pulmonary shunt, the approach was to use the natural AP window but limit overcirculation with a fenestrated patch. This approach is aimed at reducing pulmonary blood flow and preserving pulmonary artery architecture. A l-day-old female infant, weighing 2420 gm, was transferred to Texas Children’s Hospital for evaluation of cyanosis and multiple congenital anomalies. The patient was a full-term product born to a 30-year-old gravida 2, para 2 mother by cesarean section due to abruptio placenta. On admission, the patient was intubated and mechanically ventilated. She was minimally cyanotic. The precordium was quiet with a normal first heart sound and a single and slightly accentuated second heart sound. A grade II/VI crescendo-decrescendo systolic murmur was followed by a diastolic rumble along the left sternal border. The remainder of the examination was significant for imperforate anus, absent left radius, and absent left thumb. Chest radiogram showed mild cardiomegaly, increased pulmonary
Volume Number
123 1
Brief Communications
261
Fig. 2. Postoperative two-dimensional echocardiogram with color-flow interrogation from the suprasternal notch view. The patch across the AP window (open arrows) is visualized with a turbulent jet from the ascending aorta (AO) to the main pulmonary artery (MPA) across the surgically created central fenestration.
vascular markings, and hemivertebrae. Two-dimensional echocardiographic examination showed tricuspid atresia type 1B (normally related great arteries [type l] with small and restrictive ventricular septal defect [type B]). The subpulmonary infundibulum and the pulmonary valve were hypoplastic. A large AP window extended from immediately above the pulmonary sinuses of Valsalva to the origin of the right pulmonary artery. The AP window was best visualized in the parasternal short-axis view and from the suprasternal view (Fig. 1). The main pulmonary artery and branches were well developed. Pulsed Doppler and color flow interrogation demonstrated prograde systolic flow through the hypoplastic pulmonary valve into the main pulmonary artery and left-to-right shunting across the AP window. Cardiac catheterization confirmed the echocardiographic diagnosis. The systolic pressure in the left ventricle, aorta, and main pulmonary artery were equal and the systemic arterial blood oxygen saturation was 89 % . In the next 2 weeks, the patient developed progressive congestive heart failure accompanied by bounding peripheral pulses. At 18 days of age, she was taken to the operating room and, via median sternotomy and low-flow cardiopulmonary bypass with cardioplegia, the AP window was closed with a glutaraldehyde-treated pericardial patch, which was then centrally perforated, thus creating an approximately 3 mm aortopulmonary fenestration. The atria1 septal defect was also enlarged. The postoperative course was remarkable for Serratia marcescens sepsis, which re-
solved with antibiotic treatment. Transverse colostomy for the imperforate anus and duodenoduodenostomy for a duodenal web were also performed. Follow-up echocardiograms showed turbulent left-to-right flow across the fenestrated patch, with a peak systolic velocity of 5 m/set (Fig. 2). The patient was discharged from the hospital at 47 days of age without evidence of heart failure; before discharge she had begun to gain weight. AP window is considered to result from failure of the aortopulmonary septum to completely divide the aortic sac into the aorta and pulmonary artery.5 Interestingly, the majority of previously reported associated cardiac malformations involved the conotruncus and aortic arches 4 and 6. We were unable to find reported cases with the coexistence of AP window and anomalies of the atrioventricular canal such as was found here-i.e., malformations of the mitral and/or tricuspid valve or the septum of the atrioventricular canal. The significance of this observation remains unknown. The clinical presentation and the initial course in this rare anomaly were characterized by mild cyanosis and increased pulmonary blood flow caused by leftto-right shunting across the AP window. The rapidly progressive congestive heart failure that followed the decline in pulmonary vascular resistance mandated surgical intervention to limit pulmonary blood flow while preserving the architecture of the pulmonary arteries. This was considered to be of particular importance in lieu of a future modified Fontan operation. The objectives of this first-stage
262
Brief Communications
American
palliative procedure were successfully achieved by closing the AP window with a pericardial patch, leaving a 3 mm central fenestration to serve as a controlled aortopulmonary shunt. This fenestration should be easily patch-closed during definitive surgery. The use of a fenestrated patch as a way to control systemic-to-pulmonary blood flow was previously suggested by Dr. Richard Jonas as part of an alternative palliation for the hypoplastic left heart syndrome.‘j We believe that this palliation will allow this patient to grow and will alIow a safer definitive repair at a later time. REFERENCES
1. 2. 3.
4. 5.
6.
Marquis RM. Aorta-pulmonary defect. In: Watson H, ed. Paediatric cardiology. St. Louis: CV Mosby Co, 1968:286-90. Blieden LC, Moller JH. Aorticopulmonary aeptal defect. An experience with 17 patients. Br Heart J 1974;36:630-5. Kirklin JW, BarratcBoyes BG. Aortopulmonary windows. In: Kirklin JW. Barrat-Boves BG. eds. Cardiac sureerv. - < New York: John Wiley & Sons, 19861933-7. Elliotson J. Case of malformation of the pulmonary artery and aorta. Lancet 183%1:247-g. Tabak C, Moskowitz W, Wagner H, Weinberg P, Edmunds HL. Aortopulmonary window and aortic isthmic hypoplssia. J Thorac Cardiovasc Surg 1983;86:273-9. Sade RM, Crawford FA, Fyfe DA. Symposium on hypoplastic left heart syndrome. J Thorac Cardiovasc Surg 1986;91:937-9.
Bilateral femoral neuropathy caused by iliacus hematomas during anticoagulation after cardiac catheterization Xavier Daniel
Puechal, MD, Frederic Liote, Kuntz, MD. Paris, France
MD, and
Hemorrhage in one iliacus muscle with resulting femoral nerve palsy is a well-known complication in hemophiliacs, or in patients undergoing anticoagulant therapy.’ However, a bilateral iliacus hematoma has occasionally been described.‘, 2 We report a patient with such a complication during heparin treatment after bilateral femoral vascular access for cardiac catheterization. A 63-year-old man was admitted to the Cardiology Intensive Care unit on July 2,1966, with acute inferobasal myocardial infarction. Heparin was started intravenously and was only discontinued during catheterization for short periods of time. Coagulation tests were within normal limits under anticoagulant treatment. On July 4, a cardiac catheterization was performed through the right femoral From the Department of Rheumatology, Centre Viggo Petersen, HBpital LariboieiBre. Reprint requests: Dr. F. LiotC, Department of Rheumatology, Centre Viggo Petersen, Hapital LeriboiiSre, 6, rue Guy Patin, F-75010 Paris, France. 4/4/33402
January 1992 Heart Journal
artery. On July 24., he began to complain of some discomfort in the area of the right anterior thigh and of muscle weakness. Two days later, a percutaneous transcoronary angioplasty was performed using the left femoral artery for access. Following angioplasty, he experienced severe pain in the left anterior thigh and noticeable weakness without local ecchymosis. During the following days, the patient was seen in the Department of Rheumatology. Weakness was noticed in both psoas and quadriceps muscles, while the function of all distal muscles was normal. There was an area of hypoesthesia along the medial border of both thighs and an absence of a patellar reflex. There was no swelling and no change in skin color. The computed tomography (CT) scan of the pelvis revealed two large masses corresponding to a voluminous bilateral bleeding into the iliacus and psoas muscles (Fig. 1). As there was progressive motor recovery of the quadriceps muscles, no surgical decompression was proposed. At 4 weeks’ follow-up, after intensive physiotherapy, no more muscular weakness was observed, but mild pain and hypoesthesia persisted. Two years later, his examination was uneventful. Sudden pain, usually in the inguinal region, is always the first symptom of femoral neuropathy secondary to intrapelvic hematoma. Signs of femoral nerve palsy rapidly develop after the onset of pain, together with a diminished patellar reflex. As reported in a review of the literature including 129 cases of intrapelvic hematomas,3 a characteristic phenomenon is the inconstant contracture of the hip (30% ), which is flexed, abducted, and rotated externally. The clinical pattern can include a mass in the iliac fossa (51%), ecchymosis in the inguinal area or femoral canal (13 % ), a drop of hematocrit (40 %), and hypovolemic shock (22%).3 A bilateral presentation13 2 is less widely recognized, and should arouse the possibility of an intrarachidian hematoma complicating anticoagulant therapy, which requires urgent operative decompression. In patients without coagulation disturbances, femoral neuropathy caused by iliacus hematoma rarely occurs. The causes are usually traumatisms. A report of a large cooperative study on cardiac catheterization4 contained only one case of femoral nerve injury in a total of 12,367 procedures. Another report5 including 5306 percutaneous punctures of the femoral vein for hemodialysis mentioned only one damaged femoral nerve. However, such an injury may result either from a hematoma or from a direct traumatic nerve lesion caused by the tip of the guide wire or catheter at the time of insertion. In patients undergoing anticoagulant therapy, an overdose was not apparent in one third of the cases.3 A previous femoral artery puncture was mentioned in the literature in six cases,3 as in this present case. In our patient, the cause of the iliacus hematomas is a bilateral inguinal vascular perforation during the cardiac catheterization leading to large hematomas, provoked by anticoagulation. The femoral nerve palsy is caused by compression of the nerve where it passes under the inguinal ligament2 Clinical features are the most valuable aid for diagnosis, and CT is the most sensitive method for confirmation of these hemato-
Brief Communications
American
January IS92 Heart Journal
fractionation during stimulations (Fig. 3). (4) The notch, which showed a bradycardia-dependent exaggeration, also characterizes the ECG of this patient and might be closely related to the arrhythmogenic substrate, as suggested from the change observed after the ablation procedure (Fig. 1, A and B). The outcome of an attempt at catheter ablation was excellent, and the patient is waiting for a reevaluation examination. Furthermore, use of the AICD will now be indicated. REFERENCES 1. Mmorwski
M, Reide
PR, Mower
MM,
et al. Termination
malignant ventricular arrhythmias with implantable lator in human beings. N Enel 2. Josephson ME, Horowitz LN, Greenspan AM. Role of catheter
evaluation
of ventricular
of
defibril-
J Med 1980:303:322-4. Spielman SR, Waxman HL, mapping in the preoperative
tachycsrdia.
Am J Cardiol 1982;
49207-20. 3. Aizawa Y, Satou M, Funaxaki T, Aiiawa M, Suzuki K, Shibata A, Josephson ME. Early experiences of endocardial catheter mapping of the left ventricle in sustained ventricular tachy-
cardia. Efficacy, safety and complication. 51:1283-g 4. Niwano
S, Aizawa
Y, Satoh
M, Shibata
Jpn Circ J 1987;
A. Low energy
electri-
cal catheter ablation of sustained ventricular tachycardia originating from the right ventricle. AM HEART J 1989; 117:1155-7. 5. Benson
DW,
Benditt
DG, Anderson
RW,
et al. Cardiac
arrest
in young, ostensibly healthy patients: clinical, hemodynsmic, and electrophysiologic findings. Am J Cardiol 198%52:65-g. 6. Belhassen B, Shapga I, Schoshani D, Paredes A, Miller H, Laniado S. Idiopathic ventricular fibrillation: inducibility and beneficial effects of class I antiarrhythmic agents. Circulation
1987;75:899-16.
Tricuspid atresia associated with aortopulmonary window: Controlling pulmonary blood flow with a fenestrated patch Tal Geva, MD,* David A. Ott, MD,b Achi Ludomirsky, MD,a Susan J. Argyle, MD, and Martin P. O’Laughlin, MD.” Houston, Texas
Aortopulmonary (AP) window is an uncommon anomaly, with an incidence of less than one per 1000 cases of congenital heart disease. l-3 The defect, first reported in 1820,4 is associated with other cardiovascular malformations in one third to one half of cases. The most frequent
From *the Lillie Frank Abercrombie Section of Pediatric Cardiology, Department of Pediatrics, Baylor College of Medicine and Texas Children’s Hospital; and bthe Department of Thoracic and Cardiovascular Surgery, St Luke’s Episcopal Hospital, Texas Children’s Hospital, Texas Heart Institute. Reprint Hospital,
requests: Houston,
4/4/33327
Tal Geva, MD, TX 77030.
Pediatric
Cardiology,
Texas
Children’s
Fig. 1. Two-dimensional echocardiogram from the high left parasternal short-axis view showing the ascending aorta (AO), main pulmonary artery (MPA), and its bifurcation. The large aortopulmonary window (arrow) involves the proximal segments of the great arteries.
association has been with patent ductus arteriosus, followed by ventricular septal defect, tetralogy of Fallot, subaortic stenosis, coarctation of the aorta, interrupted aortic arch, anomalous origin of the right or left coronary artery from the pulmonary artery, anomalous origin of the right pulmonary artery from the aorta, and bicuspid aortic valve.3 The coexistence of an AP window with tricuspid atresia has not previously been documented. We report a case of tricuspid atresia with an AP window. Since the infant had tricuspid atresia with subvalvar and valvar pulmonary stenosis, she required augmented pulmonary blood flow; rather than closing the AP window and creating a new systemic-to-pulmonary shunt, the approach was to use the natural AP window but limit overcirculation with a fenestrated patch. This approach is aimed at reducing pulmonary blood flow and preserving pulmonary artery architecture. A l-day-old female infant, weighing 2420 gm, was transferred to Texas Children’s Hospital for evaluation of cyanosis and multiple congenital anomalies. The patient was a full-term product born to a 30-year-old gravida 2, para 2 mother by cesarean section due to abruptio placenta. On admission, the patient was intubated and mechanically ventilated. She was minimally cyanotic. The precordium was quiet with a normal first heart sound and a single and slightly accentuated second heart sound. A grade II/VI crescendo-decrescendo systolic murmur was followed by a diastolic rumble along the left sternal border. The remainder of the examination was significant for imperforate anus, absent left radius, and absent left thumb. Chest radiogram showed mild cardiomegaly, increased pulmonary
Volume Number
123 1
Brief Communications
261
Fig. 2. Postoperative two-dimensional echocardiogram with color-flow interrogation from the suprasternal notch view. The patch across the AP window (open arrows) is visualized with a turbulent jet from the ascending aorta (AO) to the main pulmonary artery (MPA) across the surgically created central fenestration.
vascular markings, and hemivertebrae. Two-dimensional echocardiographic examination showed tricuspid atresia type 1B (normally related great arteries [type l] with small and restrictive ventricular septal defect [type B]). The subpulmonary infundibulum and the pulmonary valve were hypoplastic. A large AP window extended from immediately above the pulmonary sinuses of Valsalva to the origin of the right pulmonary artery. The AP window was best visualized in the parasternal short-axis view and from the suprasternal view (Fig. 1). The main pulmonary artery and branches were well developed. Pulsed Doppler and color flow interrogation demonstrated prograde systolic flow through the hypoplastic pulmonary valve into the main pulmonary artery and left-to-right shunting across the AP window. Cardiac catheterization confirmed the echocardiographic diagnosis. The systolic pressure in the left ventricle, aorta, and main pulmonary artery were equal and the systemic arterial blood oxygen saturation was 89 % . In the next 2 weeks, the patient developed progressive congestive heart failure accompanied by bounding peripheral pulses. At 18 days of age, she was taken to the operating room and, via median sternotomy and low-flow cardiopulmonary bypass with cardioplegia, the AP window was closed with a glutaraldehyde-treated pericardial patch, which was then centrally perforated, thus creating an approximately 3 mm aortopulmonary fenestration. The atria1 septal defect was also enlarged. The postoperative course was remarkable for Serratia marcescens sepsis, which re-
solved with antibiotic treatment. Transverse colostomy for the imperforate anus and duodenoduodenostomy for a duodenal web were also performed. Follow-up echocardiograms showed turbulent left-to-right flow across the fenestrated patch, with a peak systolic velocity of 5 m/set (Fig. 2). The patient was discharged from the hospital at 47 days of age without evidence of heart failure; before discharge she had begun to gain weight. AP window is considered to result from failure of the aortopulmonary septum to completely divide the aortic sac into the aorta and pulmonary artery.5 Interestingly, the majority of previously reported associated cardiac malformations involved the conotruncus and aortic arches 4 and 6. We were unable to find reported cases with the coexistence of AP window and anomalies of the atrioventricular canal such as was found here-i.e., malformations of the mitral and/or tricuspid valve or the septum of the atrioventricular canal. The significance of this observation remains unknown. The clinical presentation and the initial course in this rare anomaly were characterized by mild cyanosis and increased pulmonary blood flow caused by leftto-right shunting across the AP window. The rapidly progressive congestive heart failure that followed the decline in pulmonary vascular resistance mandated surgical intervention to limit pulmonary blood flow while preserving the architecture of the pulmonary arteries. This was considered to be of particular importance in lieu of a future modified Fontan operation. The objectives of this first-stage
262
Brief Communications
American
palliative procedure were successfully achieved by closing the AP window with a pericardial patch, leaving a 3 mm central fenestration to serve as a controlled aortopulmonary shunt. This fenestration should be easily patch-closed during definitive surgery. The use of a fenestrated patch as a way to control systemic-to-pulmonary blood flow was previously suggested by Dr. Richard Jonas as part of an alternative palliation for the hypoplastic left heart syndrome.‘j We believe that this palliation will allow this patient to grow and will alIow a safer definitive repair at a later time. REFERENCES
1. 2. 3.
4. 5.
6.
Marquis RM. Aorta-pulmonary defect. In: Watson H, ed. Paediatric cardiology. St. Louis: CV Mosby Co, 1968:286-90. Blieden LC, Moller JH. Aorticopulmonary aeptal defect. An experience with 17 patients. Br Heart J 1974;36:630-5. Kirklin JW, BarratcBoyes BG. Aortopulmonary windows. In: Kirklin JW. Barrat-Boves BG. eds. Cardiac sureerv. - < New York: John Wiley & Sons, 19861933-7. Elliotson J. Case of malformation of the pulmonary artery and aorta. Lancet 183%1:247-g. Tabak C, Moskowitz W, Wagner H, Weinberg P, Edmunds HL. Aortopulmonary window and aortic isthmic hypoplssia. J Thorac Cardiovasc Surg 1983;86:273-9. Sade RM, Crawford FA, Fyfe DA. Symposium on hypoplastic left heart syndrome. J Thorac Cardiovasc Surg 1986;91:937-9.
Bilateral femoral neuropathy caused by iliacus hematomas during anticoagulation after cardiac catheterization Xavier Daniel
Puechal, MD, Frederic Liote, Kuntz, MD. Paris, France
MD, and
Hemorrhage in one iliacus muscle with resulting femoral nerve palsy is a well-known complication in hemophiliacs, or in patients undergoing anticoagulant therapy.’ However, a bilateral iliacus hematoma has occasionally been described.‘, 2 We report a patient with such a complication during heparin treatment after bilateral femoral vascular access for cardiac catheterization. A 63-year-old man was admitted to the Cardiology Intensive Care unit on July 2,1966, with acute inferobasal myocardial infarction. Heparin was started intravenously and was only discontinued during catheterization for short periods of time. Coagulation tests were within normal limits under anticoagulant treatment. On July 4, a cardiac catheterization was performed through the right femoral From the Department of Rheumatology, Centre Viggo Petersen, HBpital LariboieiBre. Reprint requests: Dr. F. LiotC, Department of Rheumatology, Centre Viggo Petersen, Hapital LeriboiiSre, 6, rue Guy Patin, F-75010 Paris, France. 4/4/33402
January 1992 Heart Journal
artery. On July 24., he began to complain of some discomfort in the area of the right anterior thigh and of muscle weakness. Two days later, a percutaneous transcoronary angioplasty was performed using the left femoral artery for access. Following angioplasty, he experienced severe pain in the left anterior thigh and noticeable weakness without local ecchymosis. During the following days, the patient was seen in the Department of Rheumatology. Weakness was noticed in both psoas and quadriceps muscles, while the function of all distal muscles was normal. There was an area of hypoesthesia along the medial border of both thighs and an absence of a patellar reflex. There was no swelling and no change in skin color. The computed tomography (CT) scan of the pelvis revealed two large masses corresponding to a voluminous bilateral bleeding into the iliacus and psoas muscles (Fig. 1). As there was progressive motor recovery of the quadriceps muscles, no surgical decompression was proposed. At 4 weeks’ follow-up, after intensive physiotherapy, no more muscular weakness was observed, but mild pain and hypoesthesia persisted. Two years later, his examination was uneventful. Sudden pain, usually in the inguinal region, is always the first symptom of femoral neuropathy secondary to intrapelvic hematoma. Signs of femoral nerve palsy rapidly develop after the onset of pain, together with a diminished patellar reflex. As reported in a review of the literature including 129 cases of intrapelvic hematomas,3 a characteristic phenomenon is the inconstant contracture of the hip (30% ), which is flexed, abducted, and rotated externally. The clinical pattern can include a mass in the iliac fossa (51%), ecchymosis in the inguinal area or femoral canal (13 % ), a drop of hematocrit (40 %), and hypovolemic shock (22%).3 A bilateral presentation13 2 is less widely recognized, and should arouse the possibility of an intrarachidian hematoma complicating anticoagulant therapy, which requires urgent operative decompression. In patients without coagulation disturbances, femoral neuropathy caused by iliacus hematoma rarely occurs. The causes are usually traumatisms. A report of a large cooperative study on cardiac catheterization4 contained only one case of femoral nerve injury in a total of 12,367 procedures. Another report5 including 5306 percutaneous punctures of the femoral vein for hemodialysis mentioned only one damaged femoral nerve. However, such an injury may result either from a hematoma or from a direct traumatic nerve lesion caused by the tip of the guide wire or catheter at the time of insertion. In patients undergoing anticoagulant therapy, an overdose was not apparent in one third of the cases.3 A previous femoral artery puncture was mentioned in the literature in six cases,3 as in this present case. In our patient, the cause of the iliacus hematomas is a bilateral inguinal vascular perforation during the cardiac catheterization leading to large hematomas, provoked by anticoagulation. The femoral nerve palsy is caused by compression of the nerve where it passes under the inguinal ligament2 Clinical features are the most valuable aid for diagnosis, and CT is the most sensitive method for confirmation of these hemato-
