Wien jugular Thrombophlebitis]
  • Cerebral sinuvenous thrombosis: a rare complication of Lyme neuroborreliosis


    Wien jugular Thrombophlebitis

    Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page. The anatomy Wien jugular Thrombophlebitis the jugular foramen is complex.

    It contains the lower cranial nerves and major vascular structures. Tumors that develop within it, or extend into it, provide significant diagnostic and surgical challenges. In this article, we describe the anatomy of the jugular foramen and outline an imaging protocol that can differentiate between lesions, thereby aiding diagnosis and facilitating management.

    The jugular foramen JFsometimes referred to Wien jugular Thrombophlebitis the posterior foramen lacerum, is situated in the floor of the posterior fossa posterolateral to the carotid canal, between the petrous temporal bone anterolaterally and the occipital bone posteromedially Fig.

    The term foramen is not strictly accurate because the JF resembles a canal with endocranial and exocranial openings. This canal is triangular in shape with its apex pointing anteromedially. Wien jugular Thrombophlebitis distance between the outer border of the jugular fossa and the apex of the mastoid process was 23 mm; between the outer border of the jugular fossa and the tympanomastoid suture, the distance was 15 mm.

    A degree of asymmetry of the JF is common and is attributed to variability in bone formation around the primitive posterior foramen lacerum and to unequal development of the lateral sinuses. Inneren Leisten Krampfadern of the most frequently seen variations within the JF is a bony partition that has a reported prevalence of between 3.

    The JF is a complex crossroad of neurovascular structures in the Wien jugular Thrombophlebitis base. Anatomical variation in the course of the nerves and vessels adds to the complexity of this area.

    The contents of the JF are conventionally divided into the smaller pars nervosa, situated anteromedially, Wien jugular Thrombophlebitis, and the larger pars vascularis that is posterolateral, although this terminology is misleading as both contain vascular and neural structures. The pars nervosa contains the glossopharyngeal IX and Jacobsen's nerve together with the inferior petrosal sinus, Wien jugular Thrombophlebitis, whereas the pars vascularis contains the internal jugular vein, vagus Xspinal accessory XIand Arnold's nerve.

    The IX, Wien jugular Thrombophlebitis, X, and XI nerves run through the JF in a connective tissue layer that attaches the dura matter intracranially to the pericranium extracranially. Tekdemir et al 1 reported the presence of a dural septum separating the IX from the X and XI cranial nerves.

    The posterior meningeal artery also traverses the JF. This artery is usually a branch of the ascending pharyngeal artery.

    The relationship and significance of the JF to the deep fascial planes of the neck are extremely important because both infections and tumors in these spaces are often responsible for the radiographic changes. In addition, lesions distant from the skull base in the lower face can pass through it by tracking cephalad along these potential spaces. The middle layer of the deep cervical fascia buccopharyngeal fascia lies anteromedially, the deep layer of the deep cervical fascia prevertebral fascia lies posterolaterally, and the superficial layer of the deep cervical fascia lies laterally.

    All these fasciae form the carotid space. A large number of lesions may develop or are found in the JF. They arise from structures normally found within the foramen or from adjacent tissues; in other words, either intrinsically or extrinsically. The identity of most lesions can be determined by a combination of spiral computed tomography CT and magnetic resonance imaging MRI, Wien jugular Thrombophlebitis. Computed tomography is useful for analysis of JF bony margins as well as of adjacent skull base foramina.

    Tumor calcification and hyperostosis are well demonstrated with this form of examination. Magnetic resonance imaging with gadolinium shows the characteristics of a tumor, its vascularization and extension and its relationshi p to Wien jugular Thrombophlebitis structures.

    Tumor delineation can be improved using fat-suppression sequences. Magnetic resonance angiography MRA or venography can help to demonstrate the type of the tumor vascularization and Verletzung von Blut, die hatten local venous circulation.

    Digital subtraction angiography DSA Wien jugular Thrombophlebitis a prerequisite in patients with Wien jugular Thrombophlebitis vascular lesions for which preoperative embolization might be appropriate. Because the skull base presents an undulating surface and is relatively thin, section thickness must be kept to a minimum i. Coronal images are essential because the plane of the JF approximates the axial.

    The most common tumor to develop in the JF is a paraganglioma. Paragangliomas in the skull base are ubiquitous in their distribution and arise from paraganglia or glomus cells situated at the following sites: Imaging studies are necessary to depict the location and extent of tumor involvement, to help determine the surgical approach, and to predict operative morbidity and mortality. Balloon test occlusion Wien jugular Thrombophlebitis performed if the internal carotid artery is involved or encased.

    Preoperative embolization for large paragangliomas is also useful to reduce both bleeding and surgical time. Glomus jugular tumors are not encapsulated and tend to infiltrate connective tissue planes. They have a distinctive pattern of spread that helps to differentiate them from other intrinsic tumors in this region.

    Glomus jugular tumors follow the path of least resistance including mastoid air cell tracts, vascular channels, the eustachian tube, and neural foramina. Other key features are dehiscence of the Wien jugular Thrombophlebitis of the tympanic cavity and proliferation into Wien jugular Thrombophlebitis tympanum, causing destruction of the ossicles and encasement of the carotid crest. In Wien jugular Thrombophlebitis, destruction of the bony Wien jugular Thrombophlebitis and extension into the cerebellopontine or Wien jugular Thrombophlebitis angle is seen.

    Unfortunately, occasional cases are still found where the differential cannot be made, and in these the term glomus jugulotympanicum tumor is used. The size of the tumor would seem to be is inversely related to postoperative Wien jugular Thrombophlebitis nerve preservation. When the tumor extends intradurally, it tends to insinuate itself among the delicate fascicles of the involved nerves.

    Removal of tumor requires considerable manipulation of the nerves that often results in functional impairment and disruption. The presence of a sharp medial tumor border may indicate that the cranial nerves are separable from the tumor, although this is not an absolute predictor, Wien jugular Thrombophlebitis.

    The radiologist should delineate the exact extent of bone destruction and soft tissue mass to establish the likely boundaries of any surgical resection, Wien jugular Thrombophlebitis. Another hallmark of a glomus jugular tumor in both CT and MRI modalities that will help differentiate it from other tympanic mass e.

    This appearance, Wien jugular Thrombophlebitis, usually seen in tumors larger than 1 cm, Wien jugular Thrombophlebitis, is highly Wien jugular Thrombophlebitis of a glomus tumor but can also be seen in other hypervascular lesions, such as metastatic hypernephroma and metastatic thyroid carcinoma.

    After radiotherapy, the tumor may shrink and have reduced T2 signal intensity and fewer flow voids. With angiography, glomus jugular tumors Fig. Their most common feeding vessels arise from the ascending pharyngeal artery and supply the inferomedial tumor compartment. The posterior auricular, stylomastoid, and occipital Wien jugular Thrombophlebitis supply the posterolateral tumor compartment.

    Large paragangliomas may derive further feeding vessels from branches of the internal maxillary, internal carotid, or even from the contralateral carotid and vertebral, via meningeal or pial arterial branches. Pial artery supply indicates transdural spread. Retrograde jugular venography is no longer used because intravenous tumor extension can be seen with MR venography.

    Neural sheath tumors, such as schwannomas and neurofibromas, share a common site of development in the JF, Wien jugular Thrombophlebitis. The clinical presentation of neural sheath tumors of the JF varies significantly according to the tumor's growth pattern. A review of the surgical literature 18 indicated that 25 of 27 patients with schwannomas of the JF had symptoms of decreased hearing.

    The literature is replete with comments of how often neural sheath tumors of the JF have been confused with vestibular schwannomas. Hoarseness and weakness of the trapezius and sternocleidomastoid muscles are often seen in patients whose tumor is within the bone of the skull base or has extended below it. Samii et al 20 categorized JF neural sheath tumors into four groups: There are characteristic CT and MRI appearances of neural sheath Wien jugular Thrombophlebitis that aid differential diagnosis.

    In nonenhanced CT images, neural sheath tumors are isodense to the brain parenchyma and are almost indistinguishable from it. After contrast, they appear as well-demarcated vascular tumors Fig. Coronal images reconstructed from raw spiral CT data offer the advantage of an insight into the intra- and extracranial parts of the tumor.

    Bone-windowed images show a smoothly scalloped, well-corticated enlargement of the JF in contrast to Wien jugular Thrombophlebitis moth-eaten pattern that is seen with paragangliomas Fig. Unfortunately, asymmetries in the size of the JF are present in a large number of normal patients, and this can cause some confusion. Furthermore, primarily intracranial type A and extracranial type C tumors may not produce enlargement of the JF.

    Matsushima et al 21 reported that all neural sheath tumors show low uniform T1-weighted intensity usually matching that of the brainhigh T2-weighted signal, and marked or moderate contrast enhancement.

    Neural sheath tumors do not generally show internal flow voids, although flow voids may be seen at the periphery of some relatively vascular vestibular schwannomas. If in doubt, DSA will differentiate between glomus jugular and neural sheath tumors on the basis of relative vascularity. Other distinguishing features are the absence of vascular pedicle s and jugular bulb compression with neural sheath tumor, Wien jugular Thrombophlebitis. Glomus jugular tumors have pronounced vascular pedicles Kombucha von Krampfadern often invade the jugular vein with intraluminal growth Fig.

    Meningiomas develop from the leptomeninges. They are defined as primary when centered in the JF intrinsic lesions and secondary when centered in the posterior fossa with extension into the JF. Primary meningiomas of the JF are characterized by an invasive growth pattern with extensive skull base infiltration. Accurate preoperative diagnosis has important prognostic and therapeutic implications. Wien jugular Thrombophlebitis meningiomas of the JF appear to behave quite differently.

    Two growth patterns are recognized, centrifugal and en plaque. Centrifugal growth takes place in all directions and involves the middle ear, the jugular tubercle, Wien jugular Thrombophlebitis, hypoglossal canal, occipital condyle, and clivus. Extrinsic spread inferiorly into the nasopharynx and carotid space may be seen, Wien jugular Thrombophlebitis.

    Further spread superiorly along the intracranial dural reflections is characteristic of en plaque growth Figs. Theoretically, Wien jugular Thrombophlebitis, the pattern of spread allows differentiation between primary meningiomas, neural sheath tumors schwannomasand paragangliomas within the JF. As previously mentioned, paragangliomas typically involve the hypotympanum superolaterally with limited involvement of the carotid space inferiorly. Only infrequently do they extend medially into the jugular tubercle, hypoglossal canal, and clivus.

    However, the pattern of spread is not totally reliable and cannot form the basis on which to make the distinction between these entities. With CT, the meningiomas are isodense to the brain and may be difficult to see on standard imaging protocols. After contrast agent administration, marked enhancement is the rule Fig. The signal intensity with MRI varies on T1- and T2-weighted images, depending on the histological pattern, and they may be indistinguishable from other JF lesions.

    It is reported that, compared with schwannomas, meningiomas usually have a lower T2-weighted signal and a higher precontrast CT attenuation. The signal intensity of the extracranial component was higher on T1- T2- and postcontrast T1-weighted images.

    It was suggested that this might be attributable to differences in the ratio of meningioma cells and interstitial bundles of collagen between intra- and extracranial components of meningioma.

    A reliable imaging feature of meningiomas is partial calcification and infiltration of the diploic spaces within the skull base, Wien jugular Thrombophlebitis. This gives rise to characteristic hyperostosis, 25 which has a distinctive appearance compared with the bone destruction caused by paragangliomas and scalloping of the foramen by neural sheath tumors Fig.

    Cerebral sinuvenous thrombosis: a rare complication of which showed left internal jugular vein usually arising from focal thrombophlebitis with.

    Colleague's E-mail is Invalid. Wien jugular Thrombophlebitis message has been successfully sent to your colleague. Lemierre syndrome is the typical presentation of human necrobacillosis. Wien jugular Thrombophlebitis is characterized by an initial infection, progressing to septic thrombophlebitis, septicemia, and multisystem embolic necrotic abscesses.

    It is usually caused by Fusobacterium necrophorumbut its pathophysiology remains obscure. A case of bilateral Lemierre syndrome secondary to periodontitis is reported.

    A previously healthy year-old African American man presented with a 2-week history of fever, chills, dyspnea, abdominal pain and vomiting, nonbloody diarrhea, anorexia, Wien jugular Thrombophlebitis, and body aches.

    He occasionally smoked marijuana but had no pets, and denied sick contact or recent travel. Physical examination was remarkable for tachypnea, tachycardia, pyrexia, icteric sclera, dry oral mucosa, moderate-to-severe gingival inflammation, and dental caries involving the upper and lower molars. The oropharynx was clear. He had tenderness over the sternocleidomastoid muscles bilaterally, and nontender cervical lymphadenopathy.

    Chest examination revealed Wien jugular Thrombophlebitis breath sounds in both bases with fine crackles at the right base. Examination of the cardiovascular and gastrointestinal systems was significant for tenderness in the right upper quadrant with no rebound.

    Laboratory findings were significant for leukocytosis with a left shift, anemia, abnormal liver function tests, elevated creatine phosphokinase, and positive blood culture for F. Chest radiographs and computed tomography scans revealed multilobar cavitary nodular densities with pleural effusions.

    Duplex sonography of the neck demonstrated thrombosed left internal jugular vein with complete occlusion of the lumen, thrombosed left subclavian, and axillary veins with minimal blood flow.

    There was also a small thrombus in both the right internal jugular and right subclavian veins with partial occlusion of their lumina. He was prescribed penicillin, metronidazole, and anticoagulation therapy and had complete resolution of the lung lesions and marginal improvement of the bilateral neck thrombophlebitis. He was awaiting dental procedures. A case trophischen Geschwüren Jod reported of extensive bilateral septic thrombophlebitis of the deep neck veins secondary to periodontal disease.

    To the best of my knowledge, this is the first case of bilateral Lemierre Wien jugular Thrombophlebitis due to periodontal disease reported in the literature.

    It highlights the typical septic thrombophlebitis of Lemierre syndrome and its protean manifestations, such as hepatitis and rhabdomyolysis. This presentation also underscores the significance of thorough dental examinations in febrile patients. With respect to anticoagulation therapy in Lemierre syndrome, though still not established, there is some evidence of utility with no untoward effects.

    Wien jugular Thrombophlebitis syndrome is the typical presentation of human necrobacillosis characterized by a primary infection which progresses to septic thrombophlebitis, septicemia, and multisystem embolic necrotic abscesses. It is usually caused by Fusobacterium necrophorum, Wien jugular Thrombophlebitis. Its pathophysiology remains obscure. A year-old African American man presented to the emergency room with a 2-week history of fever, dyspnea, abdominal pain, Wien jugular Thrombophlebitis, vomiting, nonbloody diarrhea, Wien jugular Thrombophlebitis, anorexia, and body aches, Wien jugular Thrombophlebitis.

    He took acetaminophen as needed and Wien jugular Thrombophlebitis no known allergies. He worked as a salesman for a sports club. No history of cigarette smoking was reported, but he occasionally smoked marijuana. He denied use of intravenous drugs.

    The patient was sexually active with a single heterosexual partner. On general examination, he was jaundiced, alert, fully oriented, and appeared well nourished, but in moderate respiratory distress. His vital signs were: Systemic examination was significant for icteric sclera, dry oral mucosa, moderate-to-severe gingival inflammation, and dental caries involving the left upper and lower molars.

    There was no jugular venous distension. He had nontender cervical lymphadenopathy and marked tenderness over the Wien jugular Thrombophlebitis sternocleidomastoid muscles near the angle of the jaw.

    Examination of the cardiovascular system was only remarkable for tachycardia. The abdomen was soft with normoactive bowel sounds and tender right upper quadrant without rebound.

    There was no palpable intra-abdominal organomegaly. Pertinent laboratory findings were: Serum amylase and lipase levels were normal.

    The arterial blood gases on ambient air were normal. Urinalysis was positive for large bilirubin and moderate occult blood, Wien jugular Thrombophlebitis. Urine toxicology screen was negative, whereas serum toxicology was positive for an acetaminophen level of Red blood cell sickling test was negative. Serologic and polymerase chain reaction tests for the human immunodeficiency virus were also negative.

    Also seen were bilateral pleural effusions, right greater than left, Wien jugular Thrombophlebitis. The patient was admitted to the intensive care unit for multilobar pneumonia, acute hepatitis, and rhabdomyolysis in the setting of sepsis to exclude possible septic embolic phenomenon, Wien jugular Thrombophlebitis.

    Echocardiography demonstrated normal cardiac function with no vegetations. Abdominal ultrasonography revealed mild gallbladder wall thickening with sludge, hepatosplenomegaly, and bilateral pleural effusion. On the second hospital day, he underwent flexible bronchoscopy: Culture of the bronchoalveolar fluid was negative for bacteria, legionella, mycobacteria, and fungi. Transbronchial lung biopsy showed acute inflammation with negative staining tests and cultures. The tuberculin skin test was negative after 48 hours.

    Three sputum smears for acid-fast bacillus were negative. Viral hepatitis profile was negative. Serum ceruloplasmin level was normal. Urine legionella antigen, monospot test, and anti-mycoplasma pneumoniae immunoglobulin M were negative. Antibodies against influenza A and B viruses were not identified. Serologic screening tests for collagen vascular disease were also negative.

    The anaerobic blood culture bottle drawn on admission, before antibiotics, grew a Gram-negative bacillus after 48 hours. The patient continued to have persistent fever despite the broad-spectrum antibiotic therapy. On the sixth hospital day, he had a repeat chest CT scan Fig. There was no evidence of pulmonary venous thromboembolism. The same day, the Gram-negative bacillus was identified as F. The next day there was defervescence with improvement in the patient's general clinical status.

    A CT-guided drainage of the right pleural effusion was performed on the seventh hospital day: Also, a contrast-enhanced neck CT scan showed faintly outlined left internal jugular vein IJV with a central hypodense filling defect and peripheral marginal contrast opacification suspicious for intraluminal clot in the same venous segment.

    Duplex sonography of the neck demonstrated thrombosed left IJV with complete occlusion of the lumen, thrombosed left subclavian and axillary veins with minimal blood Wien jugular Thrombophlebitis. There was also a small thrombus in both the right IJV and right subclavian vein with partial occlusion of their lumina. Duplex sonography of the lower extremities was negative for any venous thromboembolism. Brain CT scan was negative for any lesions. Given his extensive thrombophlebitis, intravenous heparin was started.

    He had dental evaluation: On hospital day 20, he was discharged home on oral metronidazole and moxifloxacin to complete 6 weeks of antibiotic treatment. Anticoagulation with warfarin was continued upon discharge.

    He had been seen for follow-up in the pulmonary clinic, and follow-up chest radiograph Fig. Repeat duplex sonography of the neck 1 month later revealed thrombosed left internal jugular, subclavian, and axillary veins with minimal blood flow. He continued to do well and a 1-year follow-up was planned.

    In Wien jugular Thrombophlebitis, Courmont and Cade 1 described the first case of human necrobacillosis due to suppurative infection of the upper aerodigestive tract caused Wien jugular Thrombophlebitis anaerobic Streptobacilluswhich is a genus of the phylum Fusobacteria. Later inLemierre 2 reported 20 cases of anaerobic septicemias, Wien jugular Thrombophlebitis, mostly caused by F.

    Lemierre classified these cases into 6 groups, based on the focus of the primary infection: He called the first group anaerobic postanginal septicemias. This syndrome is what is regarded as the classic Lemierre syndrome. Some authors have used Wien jugular Thrombophlebitis term Lemierre syndrome for all cases of human necrobacillosis with primary foci in the head, which corresponds to Lemierre's groups 1 to 3.

    In addition, they all have a common pathology: On the basis of this designation, the Lemierre and Lemierre-like syndrome could be suggested. This may be Wien jugular Thrombophlebitis to these factors: Lemierre syndrome was rarely reported in the literature during the s and s when penicillin became available, but seemed relatively common in the preantibiotic era.

    InAlston 5 reported cases of necrobacillosis from the world literature. Of great interest is the fact that among these were cases with primary skin infections. With the emergence of community-acquired methicillin-resistant Staphylococcus aureusthis is important for diagnostic discrimination and appropriate therapy, as both community-acquired methicillin-resistant Wien jugular Thrombophlebitis. Lemierre syndrome affects various age groups. The age distribution varies with the primary focus of infection.

    This syndrome affects children with otitis media, adults with tooth infections, all ages with sinusitis or mastoiditis, Wien jugular Thrombophlebitis, and older adults with predisposing diseases, Wien jugular Thrombophlebitis, and affects portal of entry distal to the head. Lemierre syndrome is most commonly caused by F. Other organisms that have been isolated in patients with Lemierre syndrome include Fusobacterium nucleatumStreptococcus spp.

    Centeral venous cath. (internal jugular vein).wmv1

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