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A case of parasellar chondromyxofibroma with ipsilateral total internal carotid artery occlusion is presented. Its radiological appearance and its pathological characteristics are discussed and compared with previously published reports. The rare association with total internal carotid artery occlusion is reviewed.
Two women requiring assisted reproduction had cervical stenosis on diagnostic evaluation. Office hysteroscopy was performed with paracervical block supplemented with mild intravenous sedation. When cervical pathology precluded placement of a diagnostic hysteroscopy, an Echosight Patton coaxial catheter with an outer echogenic sheath (5.7F) and inner 0.018-inch diameter guidewire with coude tip was introduced transcervically. Intraoperative transvaginal ultrasound was performed to ensure proper placement into the uterine cavity. When the uterine cavity was identified, cervical pathology was corrected with a VersaPoint electrosurgical electrode with bipolar coagulation through an operative hysteroscope. Concomitant diagnostic laparoscopy was not necessary. Echosight Patton coaxial catheter-guided ultrasound is a reassuring method to confirm hysteroscopic placement.
Recent studies have investigated the detection of significant arterial stenoses through identification of the "pulsus tardus" phenomenon in Doppler waveforms obtained distal to the stenosis. The etiology of this phenomenon, however, has not yet been determined. Using an in vitro model based upon an electrical circuit analogy, the authors had as their objective to determine whether the compliance of the vessel wall immediately distal to a stenosis, in conjunction with the stenosis, is the cause of pulsus tardus. For a constant stenosis, it was found that the degree of pulsus tardus, as quantitated by the acceleration index, increased as the compliance of the poststenotic segment increased. It is concluded that pulsus tardus distal to an arterial stenosis is likely due to the compliance of the normally distensible artery, in conjunction with the stenosis. Pathological conditions that alter the compliance of the poststenotic segment may affect the degree of pulsus tardus, perhaps limiting its usefulness for upstream stenosis detection.
To explicate the relationship and the clinical signification between the normal or narrow lateral recesses and the nerve roots, we measured the diameter of the entrans zone of the lateral recess, the interval between the upper articular processes and the interval between the nerve root and ab line on 50 normal cases, 43 narrow cases and 32 stenosis cases with VIDS image analysis system. The results showed that the nerve root was in the center side of the ab line in the normal station, with the degrees of the degeneration and cohesion ncreasing, the nerve root was in the lateral recess side of the ab line, and was compressed by the lateral recess. The authors considered that the real clinical signification of the entrance zone of the lateral recess was danger to the nerve root, but the deciding factors were the degrees of the degeneration and cohesion of the upper articular processes. The pathological conditions that resulted in the stenosis of the lateral recess and dangered the nerve root such as disc, flavum ligament and posterior port of the fibra ring were discussed in the article.
This review is devoted to the cellular biology of the arterial wall, particularly of the cerebral arteries. Starting with the description of the structure and physiology of normal arteries and of atherosclerotic lesions some of the current theories on the mechanisms of atherosclerosis are considered. They have developed along two lines of thinking according to whether the main role is given to arterial smooth muscle cells or to macrophage cells. Both hypotheses view atherosclerosis as a pathological deviation from a physiological reaction aimed at maintaining and repairing the permanently strained arterial intima. The risk factors, as identified by epidemiological studies, are likely to play a major role in this degenerative process.
The nutcracker's syndrome or phenomenom is defined as the left renal vein compression between the aorta and the superior mesenteric artery. Diagnosis is uncommon, not only due to its low frequency but for the dificulty to be suspected in usual findings as lumbar pain or hematuria. We present the case of a patient to whom we were able to show mentioned pathology with the helicoidal TC with volumetric reconstruction "3D" (VR).
The importance of secretory immunoglobulin A (IgA) of local immune defense in the gastrointestinal tract has gained increasing acceptance. Bacterial contamination is a major factor related to mortality in acute pancreatitis. However, very little is known about IgA in pancreatic juice. Pure pancreatic juice was collected from 40 patients undergoing pancreatoduodenectomy. The patients were divided into three groups according to the degree of preoperative pancreatic duct obstruction, as follows: normal, narrowed, and obstructed. IgA concentration, amylase activity, and daily volume of pancreatic juice were measured. Daily IgA secretion into pancreatic juice was constant during the early period after the operation. The concentration of IgA in the control group was 5 +/- 0.8 microg/ml, and IgA daily secretion was 1.2 +/- 0.2 mg/day. Pancreatic duct obstruction resulted in a marked decrease in both amylase and pancreatic juice secretion. The concentration of IgA, however, was markedly increased in the narrowed group (11.1 +/- 2.4 microg/ml) and the obstructed group (32.5 +/- 5.4 microg/ml). The concentration of amylase increased with the increase in pancreatic juice. Conversely, the concentration of IgA increased with the decrease in volume of pancreatic juice. Similarly, the increased in IgA concentrations positively correlated with the decrease in amylase activity. In conclusion, the mechanisms that modulate IgA secretion in the human pancreas are essentially different from those that modulate digestive enzyme and fluid secretion. IgA in pancreatic juice may play an important role in pathological conditions such as pancreatic duct obstruction. As such, the measurement of IgA in pancreatic juice may potentially be used as a new marker of local immune defense and exocrine pancreatic function.
Umbilical cord stricture is an uncommon but distinctive condition associated with intrauterine fetal death. Although cases have been reported periodically since the last century, there has been considerable speculation as to whether the condition is real or a postmortem artifact. In the present study, 25 cases reported since 1925 are reviewed and 8 new cases are described. Clinically, a decrease in fetal movements is usually the only symptom during the second or third trimester of pregnancy and fetal death occurs soon after. The women's age, health, and previous history have shown no link with this condition, but a higher incidence is noted in twin pregnancies. Morphologically, most infants are macerated and an extremely narrow segment of umbilical cord is usually seen at the fetal end and rarely at the placental end or in multiple sites along the cord. Absence of Wharton's jelly, stenosis, or obliteration of cord vessels at the narrow segment and intravascular cord thrombosis are the major pathological features. The findings of this study support the view that the condition can cause fetal death and alerts both pathologists and clinicians to the important features identifying this cause of perinatal wastage.
The Authors report on their cases of biliary surgery reoperation, necessary in 267 cases out of 3193 primary operations. After a short discussion of the aetiological, diagnostic and therapeutic problems of relapsing biliary pathology, they compare their results with those of the most important sets of cases reported in world literature.
Respiratory symptoms are often present in infants with congenital cardiac anomalies, but the intrinsic pathology of the airway itself or external compression by abnormal vessels is frequently undetected before cardiac repair. We collected 12 patients with airway pathology from July 1996 to October 1998; all had definite diagnosis of lesions of the airway and its adjacent vessels by preoperative ultrafast computed tomography. Four had intrinsic pathology (one retrotracheal diverticulum, three tracheal stenosis) as well as external compression. Among them, six had complete vascular ring, four partial rings and three had bronchial compression by aneurysmal dilatation of branch pulmonary arteries. Simultaneous airway repair (one diverticulectomy, three patch tracheoplasty) and external decompression were performed in ten cases under cardiopulmonary bypass, nine of ten had simultaneous cardiac repair; the other two were done before cardiac repair. All survived except three. We concluded that ultrafast computed tomography is indispensable for definite diagnosis of airway and adjacent cardiovascular pathology. Mere repair of congenital cardiac defects without rectification of the airway and its adjacent structures is incompatible with survival.
Although umbilical cord stricture and umbilical cord overcoiling have been established as causes of intrauterine fetal demise, relatively few studies addressed this issue, most of them being case reports. We reviewed a total of 268 fetal autopsies during a 3-year period from 1998 to 2001. One hundred thirty nine cases of fetal demise including spontaneous abortion were identified. Nineteen percent (26 of 139) were associated with umbilical cord stricture, overcoiling, or a combination of both. Stricture of the umbilical cord was defined as a decrease in diameter in relation of the remaining umbilical cord; overcoiling as 0.3 coil/cm or greater. Fetal demise most commonly occurred in the second trimester, with a mean gestation age of 21 weeks. The average maternal age was 33 years; 15% had a prior fetal demise. We found that 77% (20 of 26) of these cases had umbilical cord stricture only or with overcoiling, 23% (6 of 26) had umbilical cord overcoiling alone. Localized deficiency of Wharton's jelly and increased collagen were found in all cases with umbilical cord stricture with or without overcoiling. In patients with umbilical cord overcoiling alone, 25% had Wharton's jelly deficiency; half of them had increased collagen deposition in the umbilical cords. The placenta was reviewed for secondary thrombosis of the vessels of the chorionic plate. Thrombosis of the vessels of the chorionic plate was noted in 54% of the patients. Our study suggests that umbilical cord stricture and cord overcoiling may represent two distinct pathological entities commonly causing fetal demise. This observation reinforces the importance of a fetal autopsy with careful examination of the placenta and umbilical cord with documentation of the cord coil index.
The sensitivity of various criteria of the physical exercise test in revealing myocardial ischemia was studied in 2 groups of patients with ischemic heart disease: 1st group of 64 patients with normal ECG at rest, 2nd group of 96 patients with cicatricial changes in the myocardium. Selective coronography demonstrated atherosclerotic narrowing (stenosis of more than 70%) of one or more coronary arteries of the heart in all patients. During physical exercise an attack of angina pectoris without "ischemic" changes on the ECG occurred in 36.1% of patients of the 1st group and in 22.4% of patients of the 2nd group. The frequency of other clinical signs of cessation of the exercise (dyspnoea, change of arterial pressure, extrasystole and others) was three and a half times higher in patients with cicatricial changes in the myocardium. It is concluded that the frequency with which signs of myocardial ischemia are revealed during physical exercise depends not only on the pronounced character of the pathological coronary condition and the development of collateral circulation but also by the sensitivity of the separate ECG leads and the presence and localization of cicatricial changes in the myocardium.
PURPOSE: This article reviews experience with arterial injury caused by thoracic outlet syndrome. Special emphasis is placed on the influence of athletic or work activities on the axillary-subclavian artery system and the mechanism by which the humeral head compresses the axillary artery and the circumflex humeral arterial branches. METHODS: Retrospective review identified 34 patients (age range 13 to 67 years) treated for upper extremity symptoms or ischemic complications of thoracic outlet syndrome from 1983 to 1993. Evaluation included assessment of occupational and recreational activities plus duplex ultrasonography and contrast arteriography with positional maneuvers. RESULTS: Twenty-two patients (27 arms) had subclavian artery injury, which was most commonly caused by compression by a bony abnormality (cervical rib, 16; anomalous first rib, two; cervical rib and anomalous first rib, two). Fourteen of the 27 arms had distal embolization. All 27 had surgical decompression of the subclavian artery; 15 required concomitant arterial reconstruction. Twelve additional patients (nine athletes) had axillary artery involvement, all from arterial compression by the head of the humerus during abduction maneuvers; all had concomitant compression of the posterior circumflex humeral artery. Axillary arterial injury included thrombosis (one), aneurysm (two), and symptomatic extrinsic compression only (nine). Five patients with axillary artery involvement were treated without a surgical procedure; of the remainder, three underwent decompression procedures only, and four had direct arterial repair. In both groups all subclavian and axillary artery reconstructions were patent at last follow-up examination (mean 31 months). CONCLUSION: Most patients with thoracic outlet syndrome who have arterial involvement have a bony anomaly causing subclavian artery compression. This study demonstrates that humeral head compression of the axillary artery and its circumflex branches is a surprisingly common pathologic mechanism. Awareness of this condition affords a better therapeutic approach to arterial injuries caused by thoracic outlet syndrome.
UNLABELLED: Hypoperfusion of the brainstem during head rotation may be a risk factor for the development of SIDS. On this background we established a Doppler sonographic screening programme of the basilar cerebral arteries to evaluate the dependency of blood flow on head and body position. PATIENTS AND METHOD: We investigated 3840 newborns (1872 girls and 1968 boys) with a birth weight of 3399 +/- 497 g and a gestational age of 39.2 +/- 1.4 weeks. The investigations were performed in the neonatal period with an average age of 4.7 +/- 3 days. In all infants blood flow was measured in the basilar artery (BA) in supine position with the head in the midline. From the flow profile peak systolic flow velocity Vs and time average flow velocity TAV were measured. Additionally flow measurements were performed in supine and prone position with rotation of the head to the right and left side. A decrease of blood flow velocities below 50% of the value in neutral position was considered to be abnormal. Retrograde or biophasic flow profiles during rotation were considered to be pathologic. In infants with abnormal or pathologic flow during rotation of the head flow measurements in the vertebral arteries (VA) were additionally performed. Blood flow velocities in the VA were measured in supine and prone position with the head in the midline position and after rotation to the right and to the left. In neutral position unilateral vertebral hypoplasia, aplasia and normal VA were differentiated. The judgement after rotation was performed such as in the BA. RESULTS: In 3807 infants (99.14%) blood flow velocities during head rotation did not decrease below 50% of the value measured in neutral position. In 33 infants (0.86%) a decrease of blood flow velocities below 50% could be found during rotation. In 7 infants (0.18%) a pathologic flow could be found during head rotation. 27 of the 33 infants with abnormal and pathologic blood flow in the BA during rotation showed anatomic abnormalities of the VA. 20 of these infants (61%) had unilateral vertebral hypoplasia (11 right, 9 left side), 7 (21%) had unilateral vertebral aplasia (4 right, 3 left side). 32 of the 33 infants with abnormal flow in the BA showed a decrease of blood flow in the contralateral VA during head rotation. 9 infants had an abnormal, 19 a pathologic flow within the contralateral VA. In 4 infants the corresponding VA could not be measured during head rotation. The decrease of blood flow velocities in the BA during head rotation was caused by compression of the contralateral VA at the craniocervical junction. CONCLUSION: Blood flow within the basilar artery of healthy infants is independent of body position and rotation of the head. A decrease of the flow velocities below 50% during rotation has to be considered as an abnormality. The incidence of pathologic blood flow during head rotation with 1.8@1000 approximates the incidence of SIDS. Hypoperfusion of the brainstem during head rotation may be a risk factor of SIDS.
The purpose of this paper is to call attention to the previously overlooked entity, stenosing tenosynovitis of the flexor hallucis longus tendon in the sesamoid area of the great toe. Nine patients have been tabulated and successfully treated during the past 4 years, with an average 2 1/2-year follow-up. Trauma seems to be the causative factor. Five cases had accompanying pathology. Three cases responded to inflation of the tendon sheath with 1% lidocaine anesthesia, but the remainder required tenolysis of the sheath plus surgery to the accompanying pathology for relief. Early recognition of this problem and prompt inflation with lidocaine may be the only required treatment if this is the only entity. Chronic cases will respond to tenolysis. A plantar full visualization surgical approach is recommended.
Fifty-nine patients survived for more than 1 month after an arterial switch operation (ASO). Diagnoses in these patients included transposition of the great arteries in 27, transposition of the great arteries with ventricular septal defect in 28, and double-outlet right ventricle in four. There were six late deaths (10%) during the follow-up period, and all of them occurred suddenly and unexpectedly. Four of the six late deaths were in patients who had undergone ASO in the neonatal period. Late deaths occurred from 40 days to 10 months after the operation. Autopsies were performed in all six patients. The cause of these late deaths was acute myocardial infarction. Five patients died of subendocardial infarction resulting from stenosis of the left main coronary artery. On pathologic examination, a fibrocellular intimal thickening was noted at the proximal region of the right and left coronary arteries, which resulted in 80% stenosis on average.
The vascular system undergoes remodeling throughout life, first as primitive vessels form and reorganize, then as the circulation accommodates changing tissue perfusion requirements. Recent investigations that have targeted receptor tyrosine kinases have elucidated fundamental mechanisms that are involved in early formation and restructuring of blood vessels. Distinct receptors for vascular endothelial growth factor, and other receptor tyrosine kinases, appear to regulate very different aspects of early vessel formation including endothelial cell differentiation, tube formation and differentiation of blood vessels into microvasculature versus large vessels. In later development and in the adult circulation, remodeling adapts arteries to chronic changes in hemodynamic function. Furthermore, novel findings of how vascular cells transduce the hemodynamic forces to which they respond have been reported. Force-sensitive gene transcription occurs by previously characterized transcription factors that bind to both established and novel responsive elements in promoter regions of relevant genes. There now is evidence that more than one of these factors can regulate gene expression in response to a single physical force (shear stress). Recent studies have emphasized the role of matrix degradation and cell death, in addition to matrix synthesis and cell proliferation, in arterial remodeling. The importance of cell death and matrix degradation has also been emphasized in the pathogenesis of vascular pathologies. As a result of these and other findings, the role tissue remodeling is being examined closely as a primary factor in the pathogenesis of atherosclerosis, hypertension and restenosis after angioplasty.
We review our results in treating 5 patients with parotid duct pathology (3 stenoses, 2 calculi), using digital subtraction imaging for sialography, and standard interventional techniques using balloon catheters. Good technical results were achieved in all 5 patients. We describe our techniques and how they were modified to overcome various difficulties.