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At least 19 recordsLinked to original sources
PubMed2002

Intracranial hypotension as a cause of radiculopathy from cervical epidural venous engorgement: case report.

We describe the case of a 40-year-old man with spontaneous intracranial hypotension who presented with cervical radiculopathy associated with epidural venous engorgement. Epidural venous engorgement can occur secondary to intracranial hypotension and manifests intracranially as pachymeningeal venous engorgement. In the cervical spine, two cases of epidural venous engorgement due to intracranial hypotension have been reported in the literature, and neither patient presented with symptoms related to nerve compression. Epidural venous engorgement should be considered in the differential diagnosis of an enhancing epidural mass in the cervical spine. Diagnostic clues include sparing of the anterior midline and posterior aspects of the epidural space and, if present, pulsation artifact.

Adult↗
PubMed1989

Comparison of pulse oximeters: effects of vasoconstriction and venous engorgement.

The effects of cold-induced vasoconstriction and venous occlusion on the detection of induced hypoxaemia by four pulse oximeters were examined in 10 volunteers. In three further subjects vasoconstriction was maintained until at least one instrument failed to detect the induced hypoxaemia. Time taken to detect hypoxaemia was increased for all instruments to between two and three times the instrument's own control value for both vasoconstriction and venous engorgement (P less than 0.01). There was highly significant variation in detected minimum saturation between the instruments (P less than 0.001). One instrument failed to detect the full extent of desaturation under the experimental conditions and was more likely to fail completely to detect desaturation than the other test instruments when influenced by vasoconstriction (P less than 0.05). Significant impairment in the performance of all the instruments tested occurred in the presence of normal pulse signals. The duration of detected reductions in oxygen saturation was not significantly affected.

Blood Circulation↗
PubMed2006

Epidural venous engorgement resulting in progressive cervical myelopathy from shunt-related intracranial hypotension. Case report and review of the literature.

The authors report an unusual case of engorged epidural veins causing progressive cervical myelopathy after long-term cerebrospinal fluid (CSF) shunt therapy and intracranial hypotension. An 18-year-old woman, who had previously undergone shunt placement with a distal slit valve for a porencephalic cyst when 2 years of age, presented with progressive spastic quadriparesis, numbness, and gait difficulty. Postural headaches were absent and a lumbar puncture revealed low CSF pressure. Neuroimaging disclosed markedly engorged anterior epidural veins causing compression of the cervical spinal cord. The slit-valve shunt system was surgically removed and an external drain was placed. The patient's CSF pressure was gradually raised to clinically tolerable levels. Once the optimal pressure was identified, a programmable shunt was placed with the valve set at the same level. The patient's neurological status improved, and the epidural veins had returned to their normal size on follow-up imaging. The authors describe the unique treatment strategy used in this patient and review the literature on epidural venous engorgement as it relates to intracranial hypotension.

Adolescent↗
PubMed1992

Venous engorged tissue flaps treated with medicinal leeches.

We evaluated the ability of leeches to improve the tolerance of pedicle flaps to periods of venous congestion. Axial pedicle flaps were created on 14 rabbit ears; the venous circulation of each flap was compromised with a suture ligature. Medicinal leeches were applied to seven flaps; the other seven flaps were untreated. Tissue viability was assessed by both clinical examination and fluorometric analysis of fluorescein dye delivery. Leech-treated flaps showed poorer reperfusion than untreated flaps. No statistically significant difference was found in comparing the two groups.

Animals↗
PubMed1999

[Evolution of angiographic signs of venous hypertension and clinical signs of intracranial hypertension in intracranial dural arteriovenous fistulas].

Dural arteriovenous fistulas (dAVFs) can cause cerebral venous hypertension (VHT). The most common mechanism is due to the fact that some dAVFs can drain retrogradelly in cortical (better defined as leptomeningeal) veins (directly or after drainage in a dural sinus) causing venous engorgement and consequently an impairment of the cerebral venous drainage. However, more rarely, dAVFs without a cortical venous drainage can also be responsible for VHT probably due to dAVF shunts causing insufficient antegrade cerebral venous drainage. In addition, dAVFs are often associated with stenosis and/or thrombosis of dural sinus(es) which can worsen the VHT. Raised pressure within the superior sagittal sinus causes impeded cerebrospinal reabsorption in the arachnoid villi allowing increased intracranial pressure. The venous engorgement in the cortical veins can cause a venous congestive encephalopathy analogous to the venous congestive myelopathy of the spinal dural AVFs. Clinically VHT can cause not only symptoms related to increased intracranial pressure but also seizures, neurological deficits, impairment of the cognitive functions and dementia. An important aspect is the risk of hemorrhage in dAVFs with a leptomeningeal venous drainage leading to VHT. Although the term VHT sensu strictu should be used if venous pressure measurements are performed, angiographic criteria for VHT such as delayed circulation time, venous engorgement and abnormal visualization of the cerebral veins are well established. The purpose of our study was to evaluate the angiographic signs of VHT in patients with dAVF and to study the course of the VHT and of the clinical signs of increased intracranial pressure before and after dAVF endovascular treatment. A retrospective chart analysis of 22 patients (13 males, 9 females) ranging in age from 20 to 87 years (mean: 53 ys.) with a dAVF associated with angiographic signs of VHT was performed. Ten dAVFs were located on the transverse/sigmoid sinus(es), 6 on the superior sagittal sinus, 3 on the petro-tentorial incisura, 1 on the inferior petrosal sinus, 1 on the anterior ethmoidal region and 1 on the Galen vein region. All dAVFs had a retrograde leptomeningeal venous drainage. Stenosis or thrombosis of the dural AVF sinus was observed in 17 cases and stenosis or thrombosis of another sinus(es) and/or of the jugular vein in 8 cases. In 11 patients, the angiographic signs of VHT were global affecting the entire cerebral venous drainage and, in the other 11 patients, the VHT was focal. The VHT caused clinical symptoms of increased intracranial pressure in 18 patients. Other clinical findings included: bruit (11 cases), seizures (3 cases), vertigo (3 cases), visual deficits (2 cases) and impairment of cognitive functions (4 cases). Three patients presented hemorrhage (one parenchymal hematoma, one hemorrhagic infarction and one subarachnoid hemorrhage). The 4 patients without clinical symptoms of increased intracranial pressure presented only bruit in 2 cases, bruit and vertigo in 1 case, bruit and hemorrhagic infarction in another one. The dAVFs were treated by endovascular therapy (arterial approach: 3 cases, venous approach: 6 cases and both arterial and venous approach: 13 cases). Endovascular sessions ranged from 1 to 7 (mean: 2.8) for each patient. After the endovascular treatment, in 12 patients with complete occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cure were observed. In 8 patients with partial occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cure were observed in 4 cases (almost complete dAVF occlusion in 2 cases); in the other 4 cases, only reduction the angiographic signs of VHT and clinical improvement were obtained. In all 16 patients who were clinically cured angiographic signs of VHT disappeared despite the persistence of dAVF shunts as observed in 4 cases. (ABSTRACT TRUNCATED)

Adult↗
PubMed1998

Leech-borne Serratia marcescens infection following complex hand injury.

Leeches are commonly used in the postoperative course of plastic surgical operations where there is venous congestion in a pedicled or free flap. They provide a temporary relief to venous engorgement whilst venous drainage is re-established. It is known that leeches can carry Aeromonas hydrophila infection, and a second or third generation cephalosporin antibiotic has traditionally been given as prophylaxis against infection. We report a new observation that leeches can carry Serratia marcescens and give rise to clinically significant infection. The implication for prophylaxis and treatment of leech-associated cellulitis is discussed.

Adult↗
PubMed2006

Intractable radicular and low back pain secondary inferior vena cava stenosis associated with Budd-Chiari syndrome: endovascular treatment with cava stenting: case report and review of the literature.

STUDY DESIGN: The present report describes treatment of enlarged lumbar epidural veins in a patient with Budd-Chiari syndrome presenting with intractable radicular and low back pain. OBJECTIVE: To present a rare cause of radicular pain. To offer a case successfully to be treated with stenting of inferior vena cava stenosis. SUMMARY OF BACKGROUND DATA: Epidural venous engorgements due to inferior vena cava thrombosis have been described previously in the literature. To the authors' knowledge, this is the first case of inferior vena cava stenosis to be treated with stenting. METHODS: An 27-year-old woman presented with intractable radicular and low back pain refractory to medical treatment. She was diagnosed with Budd-Chiari syndrome for 23 years. A venography revealed severe stenosis at the hepatic portion of the inferior vena cava causing symptomatic lumbar epidural venous engorgements. RESULTS: Inferior vena cava stenosis was dilatated with endovascular stenting. Her symptoms were completely resolved after this procedure. CONCLUSIONS: Inferior vena cava stenosis related to hypertrophied caudate lobe producing lumbar epidural venous engorgements should be considered as one of the causes of radicular and low back pain. We could obtain a favorable clinical outcome by handling the primary cause of the venous engorgement.

Adult↗
PubMed2007

Ventriculoperitoneal shunt failure causing myelopathy in a patient with bilateral jugular vein occlusion. Case report.

The authors describe the case of a 36-year-old woman with bilateral internal jugular vein occlusion, hydrocephalus, and Dandy-Walker variant who presented with myelopathy that was ultimately attributed to ventriculoperitoneal (VP) shunt failure. Computed tomography (CT) angiography of the head and neck revealed epidural venous engorgement within the cervical spine, greater that 50% narrowing of the C2-5 spinal canal, and compression of the cervical spinal cord. After successful shunt revision, postoperative CT angiography revealed decreased venous engorgement as well as decompression of the cervical spinal cord, and the patient's myelopathy improved. This case represents a fascinating clinical presentation of VP shunt failure, highlighting the physiological importance of the external jugular pathways involved in cerebral venous drainage.

Adult↗
PubMed1998

Ischaemic optic neuropathy after spinal fusion.

PURPOSE: We report a case of ischaemic optic neuropathy which occurred after prolonged spine surgery in the prone position in an obese, diabetic patient. CLINICAL FEATURES: The patient was a 44-yr-old, 123 kg, 183 cm man for decompressive laminectomy and instrumented fusion of the lumbar spine. Anaesthesia was induced with thiopentone, fentanyl and succinylcholine and maintained with nitrous oxide, oxygen, isoflurane and a fentanyl infusion. He was positioned prone on the Relton-Hall frame and had an uneventful intraoperative course. Estimated blood loss was 3,000 ml. He was taken to the surgical intensive care unit (SICU) and the trachea was extubated 3.5 hr later. He had no pulmonary or haemodynamic problems and went to a regular nursing floor in the morning. He was discharged home on postoperative day #5. He telephoned his surgeon on postoperative day #7 to say that his vision had been blurry since surgery. His visual acuity was decreased, and on examination, he had a bilateral papillary defect, optic swelling and a splinter haemorrhage in the right eye. Magnetic resonance imaging (MRI) scan of the head and orbits detected no other abnormality. Based on this examination, he was felt to have bilateral ischaemic optic neuropathy and treated conservatively. By postoperative day #47, his visual acuity was greatly improved and near normal. Careful review of possible contributing factors suggests that the cause of the ischaemic optic neuropathy was venous engorgement. CONCLUSION: This patient developed ischaemic optic neuropathy from a prolonged interval in the prone position of the Relton-Hall frame, which may be related to venous engorgement.

Adult↗
PubMed1982

Retinal vein diameter during reversible upper respiratory bypass.

A reversible tracheal cannula was implanted in 14 Rambouillet sheep so that the sheep could breathe normally through the nostrils when the 'flow-through' insert was in place or through the tracheal opening when the 'bypass' insert of the cannula was in place. The outer diameter of the superotemporal retinal vein increased significantly in size during nasal bypass breathing compared to normal nasal breathing. Anteroposterior histological sections of the retina and optic disc revealed disc elevation and marked venous engorgement during nasal bypass breathing. These results suggest that a possible increase in the cerebrospinal fluid pressure during nasal bypass breathing must have caused a corresponding increase in optic nerve tissue pressure resulting in axoplasmic flow stasis and swelling of the optic nerve axons in the prelaminar area of the optic disc. The swollen axons apparently caused the compression of the thin-walled retinal veins resulting in venous engorgement.

Animals↗