scholarly journals Comparison of helical and axial mode indirect computed tomographic venography in patients with pulmonary thromboembolism

Lung India ◽  
2012 ◽  
Vol 29 (2) ◽  
pp. 131 ◽  
Author(s):  
Sameer Vyas ◽  
Ashish Bhalla ◽  
Niranjan Khandelwal ◽  
Naveen Kalra ◽  
Ashish Gupta ◽  
...  
Keyword(s):  
Pulmonary Thromboembolism ◽  
Axial Mode ◽  
Computed Tomographic ◽  
Computed Tomographic Venography

Reversal of Increased Intracranial Pressure with Removal of a Torcular Epidermoid: Case Report

Neurosurgery ◽  
2001 ◽  
Vol 48 (4) ◽  
pp. 929-932 ◽  
Author(s):  
Cornelius H. Lam ◽  
Robin K. Solomon ◽  
H. Brent Clark ◽  
Sean O. Casey
Keyword(s):  
Intracranial Pressure ◽  
Venous Obstruction ◽  
Increased Intracranial Pressure ◽  
Easy Method ◽  
Computed Tomographic ◽  
Straight Sinus ◽  
Computed Tomographic Venography ◽  
Bony Lesion ◽  
Slow Growing

Abstract OBJECTIVE AND IMPORTANCE Venous obstruction has been postulated as a cause of increased intracranial pressure, but it has been documented rarely. We present a case of obstruction of the torcula by a slow-growing epidermoid. The tumor caused increased intracranial pressure, which was relieved when it was excised. In addition, the torcular epidermoid is associated with a bifid straight sinus. CLINICAL PRESENTATION A 35-year-old man presented with a headache and a lump on the back of the head. Physical examination revealed a firm, bony lesion approximately 4 × 4 cm in size. Lumbar puncture demonstrated an intraspinal pressure of 39 cm H2O. Neuroradiological studies revealed an epidermoid that compressed and almost completely occluded the torcula. INTERVENTION After the tumor was resected, the intraspinal pressure decreased to 19 cm H2O and remained stable 6 months later. CONCLUSION Pure venous obstruction causes increased intracranial pressure. Removal of the obstruction relieves the intracranial hypertension. In addition, computed tomographic venography is a safe and easy method of documenting torcular anatomy, and it was useful in the follow-up of this patient. Computed tomographic venography can demonstrate a double straight sinus, which is a congenital variant that may be associated with the epidermoid.

The Outcome of Treatment for Pelvic Congestion Syndrome

2012 ◽  
Vol 27 (1_suppl) ◽  
pp. 74-77 ◽  
Author(s):  
P Coleridge Smith
Keyword(s):  
Lower Limb ◽  
Varicose Veins ◽  
Pelvic Congestion Syndrome ◽  
Pelvic Vein ◽  
Computed Tomographic ◽  
Computed Tomographic Venography ◽  
Clinical Series ◽  
Pelvic Varices ◽  
Pelvic Congestion

Pelvic congestion syndrome is one of many causes of chronic pelvic pain. It is generally accepted that this is attributable to ovarian and pelvic vein incompetence which may result in varices in the lower limb leading to presentation in varicose vein clinics. However, far more patients have pelvic varices associated with varicose veins in the lower limb than have pelvic congestion syndrome. Magnetic resonance imaging and computed tomographic venography are usually used in the diagnosis of this condition and criteria have been established to identify pelvic varices. Many different treatments have been used to manage the symptoms of pelvic congestion. Hysterectomy combined with oophrectomy open surgical ligation of ovarian veins and laparoscopic vein ligation have been used in the past. The most common treatments used currently involve embolization of pelvic and ovarian veins. The results of this treatment have been published in a limited number of clinical series, usually with fairly short follow-up periods. These treatments may be complicated by migration of embolization of coils used to occlude veins. The longest duration of follow-up currently reported is five years. Limited clinical evidence supports the use of embolotherapy in the management of pelvic congestion syndrome.

scholarly journals Contribution of indirect computed tomographic venography to the diagnosis of postpartum venous thromboembolism

2008 ◽  
Vol 6 (9) ◽  
pp. 1478-1481 ◽  
Author(s):  
M. P. REVEL ◽  
O. SANCHEZ ◽  
S. DECHOUX ◽  
S. COUCHON ◽  
G. FRIJA ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Computed Tomographic ◽  
Computed Tomographic Venography

Hyperhomocysteinemia Due to Pernicious Anemia Leading to Pulmonary Thromboembolism in a Heterozygous Mutation Carrier

2008 ◽  
Vol 14 (3) ◽  
pp. 365-368 ◽  
Author(s):  
Elif Küpeli ◽  
Cem Cengiz ◽  
Ayşenur Cila ◽  
Demet Karnak
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Pulmonary Thromboembolism ◽  
Lower Lobe ◽  
Pulmonary Angiography ◽  
Deficiency Anemia ◽  
Computed Tomographic ◽  
Methylene Tetrahydrofolate Reductase ◽  
Computed Tomographic Pulmonary Angiography ◽  
Methylene Tetrahydrofolate

Pulmonary thromboembolism is a life-threatening condition resulting mostly from lower extremity deep-vein or pelvic-vein thrombosis. A 46-year-old woman was admitted to hospital with pain on the right side of the chest and hemoptysis. On laboratory analysis, D-dimer level was elevated. Computed tomographic pulmonary angiography revealed intravascular filling defects due to thrombi in right lower lobe pulmonary segmental arteries. Screening for thrombophilic states was normal except for heterozygous mutations of both prothrombin and methylene tetrahydrofolate reductase (MTHFR 677) genes. Homocysteine level was high, and vitamin B12 level and serum ferritin level were reduced. Serum antiparietal antibody was positive, and therefore, pernicious anemia was diagnosed along with iron-deficiency anemia. After the diagnoses were established, enoxaparin followed by warfarin was started in addition to oral vitamin B12, pyridoxine, thiamine, folic acid, and ferroglycine sulfate supplementation. At the end of 8 weeks of the replacement therapy, vitamin B12, folate, and homocysteine levels and red cell volume were found to be normal, with complete resolution of the thrombus confirmed by repeat computed tomographic pulmonary angiography. We conclude that hyperhomocysteinemia due to vitamin B12 deficiency associated with pernicious anemia might have decreased the threshold for thrombosis. In addition, the presence of heterozygous prothrombin and methylene tetrahydrofolate reductase mutations might serve as synergistic cofactors triggering pulmonary thromboembolism.

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