Cavernous Sinus Thrombophlebitis: Case Report
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Clinical Case: Post-Procedure Thrombophlebitis
Clinical Case: Post-procedure Thrombophlebitis A 46 year old female presented with long-standing history of right lower limb fatigue and aching with prolonged standing. Symptoms –Aching, cramping, heavy, tired right lower limb –Tenderness over bulging veins –Symptoms get worse at end of the day –She feels better with lower limb elevation and application of elastic compression stockings (ECS) History Medical and Surgical history: Sjogren syndrome, mixed connective tissue disease, GERD, IBS G2P2 with C-section x2, left breast biopsy No history of venous thrombosis Social history: non-smoker Family history: HTN, CAD Allergies: None Current medications: Pantoprazole Physical exam Both lower limbs were warm and well perfused Palpable distal pulses Motor and sensory were intact Prominent varicosities Right proximal posterior-lateral thigh and medial thigh No ulcers No edema Duplex ultrasound right lower limb GSV diameter was 6.4mm and had reflux from the SFJ to the distal thigh No deep venous reflux No deep vein thrombosis Duplex ultrasound right lower limb GSV tributary diameter 4.6mm Anterior thigh varicose veins diameter 1.5mm-2.6mm with reflux No superficial vein thrombosis What is the next step? –Conservative treatment – Phlebectomies –Sclerotherapy –Thermal ablation –Thermal ablation, phlebectomies and sclerotherapy Treatment Right GSV radiofrequency ablation Right leg ultrasound guided foam sclerotherapy with 0.5% sodium tetradecyl sulfate (STS) Right leg ambulatory phlebectomies x19 A compression dressing and ECS were applied to the right lower limb after the procedure. Follow-up 1 week post-procedure –The right limb was warm and well perfused –There was mild bruising, no infection and signs of mild thrombophlebitis –Right limb venous duplex revealed no deep vein thrombosis and the GSV was occluded 2 weeks post-procedure –Tender palpable cord was found in the right thigh extending into the calf with overlying hyperpigmentation. -
Pulmonary Veno-Occlusive Disease
Arch Dis Child: first published as 10.1136/adc.42.223.322 on 1 June 1967. Downloaded from Arch. Dis. Childh., 1967, 42, 322. Pulmonary Veno-occlusive Disease K. WEISSER, F. WYLER, and F. GLOOR From the Departments of Paediatrics and Pathology, University of Basle, Switzerland Pulmonary venous congestion with or without time. She gradually became more dyspnoeic, with 'reactive' or 'protective' pulmonary arterial hyper- increasing weakness and fatigue, and her weight fell. tension (Wood, 1954; Wood, Besterman, Towers, In October 1961 she developed jaundice with acholic and McIlroy, 1957) is most commonly caused by stools and dark urine. Infective hepatitis was diagnosed, and she was put on a diet and, 2 weeks later, on corti- left heart disease. The obstruction to blood flow costeroids. She had had no known contact with a case may, however, also be located upstream to the left of hepatitis. Again, except for her dyspnoea, no cardiac atrium. Among the known causes of such obstruc- or pulmonary abnormality was found. The icterus tion are compression of the pulmonary veins by a decreased very slowly, but never disappeared entirely. mediastinal mass (Edwards and Burchell, 1951; In the following months her general condition deteriora- Andrews, 1957; Evans, 1959); congenital stenosis of ted and she was breathless even at rest. On two occasions the pulmonary veins at the veno-atrial junction she had syncopal attacks lasting a few minutes. She lost (Lucas, Woolfrey, Anderson, Lester, and Edwards, 12 kg. within one year. In January 1962 the parents finally consented to her being admitted to hospital. 1962); or thrombus formation in the pulmonary On admission she was obviously ill, wasted, jaundiced, veins due to greatly reduced blood flow associated cyanotic, and severely dyspnoeic and orthopnoeic. -
1-Anatomy of the Pituitary Gland
Color Code Important Anatomy of Pituitary Gland Doctors Notes Notes/Extra explanation Please view our Editing File before studying this lecture to check for any changes. Objectives At the end of the lecture, students should be able to: ✓ Describe the position of the pituitary gland. ✓ List the structures related to the pituitary gland. ✓ Differentiate between the lobes of the gland. ✓ Describe the blood supply of pituitary gland & the hypophyseal portal system. الغدة النخامية Pituitary Gland (also called Hypophysis Cerebri) o It is referred to as the master of endocrine glands. o It is a small oval structure 1 cm in diameter. o It doubles its size during pregnancy. lactation ,(الحمل) pregnancy ,(الحيض) A women experiences changes in her hormone levels during menstruation But only the pituitary gland will only increase in size during pregnancy .(سن اليأس) and menopause ,(الرضاعة) X-RAY SKULL: LATERAL VIEW SAGITTAL SECTION OF HEAD & NECK Extra Pituitary Gland Position o It lies in the middle cranial fossa. o It is well protected in sella turcica* (hypophyseal fossa) of body of sphenoid o It lies between optic chiasma (anteriorly) & mamillary bodies** (posteriorly). Clinical point: *سرج الحصان Anterior to the pituitary gland is the optic chiasm, so if there was a tumor in the pituitary gland or it was ** Part of hypothalamus enlarged this could press on the chiasm and disrupt the patients vision (loss of temporal field). Extra Pictures The purple part is the sphenoid bone Hypophyseal fossa Pituitary Gland The relations are important Important Relations • SUPERIOR: Diaphragma sellae: A fold of dura mater covers the pituitary gland & has an opening for passage of infundibulum (pituitary stalk) connecting the gland to hypothalamus. -
Carotid Cavernous Sinus Fistula with Central Retinal Artery Occlusion: a Case Report
Carotid cavernous sinus fistula with central retinal artery occlusion: A case report Suntaree Thitiwichienlert1, Chonwarat Phattarapongdilok1, Paiboon Bawornwattanadilok1 1Department of Ophthalmology, Faculty of Medicine Thammasat University, Thailand Background: A carotid-cavernous sinus fistula (CCF) is an abnormal arteriovenous communication between the cavernous sinus and the internal carotid artery (ICA) and/or external carotid artery (ECA). Central retinal artery occlusion (CRAO) is a rare posterior segment complication occurring as result of traumatic CCF from an ocular hypoperfusion. Case Report: We present a 58-year-old female complaining of acute visual loss, with redness and swelling of the right eye following a motor vehicle accident. Her visual acuity was light perception (PL) in the right eye and 20/40 in the left eye. The intraocular pressure (IOP) was 52 mm Hg in the right eye and normal in the left eye. Eye examinations revealed proptosis, ptosis, complete total ophthalmoplegia and a 5-mm fixed dilated right pupil with relative afferent pupillary defect (RAPD) positive in her right eye. The fundus examination showed CRAO in the right eye. Cerebral angiogra- phy revealed a high flow direct CCF Barrow’s type A. Endovascular treatment was performed using balloon embolization. During the one-year follow-up, the patient had improvement of eye redness, proptosis, and ophthalmoplegia. However, the visual prognosis was poor due to optic atrophy and macular ischemia with the final visual acuity of PL. Conclusion: A complete fundus examination found vision- threatening complications in patients who have traumatic CCFs. Early recognition of CRAO is important in the management of these patients. Conflicts of interest: The authors report no confilcts of interest. -
Treatment for Superficial Thrombophlebitis of The
Treatment for superficial thrombophlebitis of the leg (Review) Di Nisio M, Wichers IM, Middeldorp S This is a reprint of a Cochrane review, prepared and maintained by The Cochrane Collaboration and published in The Cochrane Library 2012, Issue 3 http://www.thecochranelibrary.com Treatment for superficial thrombophlebitis of the leg (Review) Copyright © 2012 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd. TABLE OF CONTENTS HEADER....................................... 1 ABSTRACT ...................................... 1 PLAINLANGUAGESUMMARY . 2 BACKGROUND .................................... 2 OBJECTIVES ..................................... 3 METHODS ...................................... 3 RESULTS....................................... 5 Figure1. ..................................... 7 Figure2. ..................................... 8 DISCUSSION ..................................... 11 AUTHORS’CONCLUSIONS . 12 ACKNOWLEDGEMENTS . 12 REFERENCES ..................................... 12 CHARACTERISTICSOFSTUDIES . 17 DATAANDANALYSES. 42 Analysis 1.1. Comparison 1 Fondaparinux versus placebo, Outcome 1 Pulmonary embolism. 51 Analysis 1.2. Comparison 1 Fondaparinux versus placebo, Outcome 2 Deep vein thrombosis. 51 Analysis 1.3. Comparison 1 Fondaparinux versus placebo, Outcome 3 Deep vein thrombosis and pulmonary embolism. 52 Analysis 1.4. Comparison 1 Fondaparinux versus placebo, Outcome 4 Extension of ST. 52 Analysis 1.5. Comparison 1 Fondaparinux versus placebo, Outcome 5 Recurrence of ST. 53 Analysis 1.6. Comparison 1 Fondaparinux -
Non-Pathological Opacification of the Cavernous Sinus on Brain CT
healthcare Article Non-Pathological Opacification of the Cavernous Sinus on Brain CT Angiography: Comparison with Flow-Related Signal Intensity on Time-of-Flight MR Angiography Sun Ah Heo 1, Eun Soo Kim 1,* , Yul Lee 1, Sang Min Lee 1, Kwanseop Lee 1 , Dae Young Yoon 2, Young-Su Ju 3 and Mi Jung Kwon 4 1 Department of Radiology, Hallym University Sacred Heart Hospital, College of Medicine, Hallym University, Seoul 14068, Korea; [email protected] (S.A.H.); [email protected] (Y.L.); [email protected] (S.M.L.); [email protected] (K.L.) 2 Department of Radiology, Kangdong Sacred Heart Hospital, College of Medicine, Hallym University, Seoul 14068, Korea; [email protected] 3 National Medical Center, Seoul 04564, Korea; [email protected] 4 Department of Pathology, Hallym University Sacred Heart Hospital, College of Medicine, Hallym University, Seoul 14068, Korea; [email protected] * Correspondence: [email protected] Abstract: Purpose: To investigate the non-pathological opacification of the cavernous sinus (CS) on brain computed tomography angiography (CTA) and compare it with flow-related signal intensity (FRSI) on time-of-flight magnetic resonance angiography (TOF-MRA). Methods: Opacification of the CS was observed in 355 participants who underwent CTA and an additional 77 participants who underwent examination with three diagnostic modalities: CTA, TOF-MRA, and digital subtraction angiography (DSA). Opacification of the CS, superior petrosal sinus (SPS), inferior petrosal sinus Citation: Heo, S.A.; Kim, E.S.; Lee, Y.; Lee, S.M.; Lee, K.; Yoon, D.Y.; Ju, Y.-S.; (IPS), and pterygoid plexus (PP) were also analyzed using a five-point scale. -
Inherited Thrombophilia Protein S Deficiency
Inherited Thrombophilia Protein S Deficiency What is inherited thrombophilia? If other family members suffered blood clots, you are more likely to have inherited thrombophilia. “Inherited thrombophilia” is a condition that can cause The gene mutation can be passed on to your children. blood clots in veins. Inherited thrombophilia is a genetic condition you were born with. There are five common inherited thrombophilia types. How do I find out if I have an They are: inherited thrombophilia? • Factor V Leiden. Blood tests are performed to find inherited • Prothrombin gene mutation. thrombophilia. • Protein S deficiency. The blood tests can either: • Protein C deficiency. • Look at your genes (this is DNA testing). • Antithrombin deficiency. • Measure protein levels. About 35% of people with blood clots in veins have an inherited thrombophilia.1 Blood clots can be caused What is protein S deficiency? by many things, like being immobile. Genes make proteins in your body. The function of Not everyone with an inherited thrombophilia will protein S is to reduce blood clotting. People with get a blood clot. the protein S deficiency gene mutation do not make enough protein S. This results in excessive clotting. How did I get an inherited Sometimes people produce enough protein S but the thrombophilia? mutation they have results in protein S that does not Inherited thrombophilia is a gene mutation you were work properly. born with. The gene mutation affects coagulation, or Inherited protein S deficiency is different from low blood clotting. The gene mutation can come from one protein S levels seen during pregnancy. Protein S levels or both of your parents. -
Carotid-Cavernous Sinus Fistulas and Venous Thrombosis
141 Carotid-Cavernous Sinus Fistulas and Venous Thrombosis Joachim F. Seeger1 Radiographic signs of cavernous sinus thrombosis were found in eight consecutive Trygve 0. Gabrielsen 1 patients with an angiographic diagnosis of carotid-cavernous sinus fistula; six were of 1 2 the dural type and the ninth case was of a shunt from a cerebral hemisphere vascular Steven L. Giannotta · Preston R. Lotz ,_ 3 malformation. Diagnostic features consisted of filling defects within the cavernous sinus and its tributaries, an abnormal shape of the cavernous sinus, an atypical pattern of venous drainage, and venous stasis. Progression of thrombosis was demonstrated in five patients who underwent follow-up angiography. Because of a high incidence of spontaneous resolution, patients with dural- cavernous sinus fistulas who show signs of venous thrombosis at angiography should be followed conservatively. Spontaneous closure of dural arteriovenous fistulas involving branches of the internal and/ or external carotid arteries and the cavernous sinus has been reported by several investigators (1-4). The cause of such closure has been speculative, although venous thrombosis recently has been suggested as a possible mechanism (3]. This report demonstrates the high incidence of progres sive thrombosis of the cavernous sinus associated with dural carotid- cavernous shunts, proposes a possible mechanism of the thrombosis, and emphasizes certain characteristic angiographic features which are clues to thrombosis in evolution, with an associated high incidence of spontaneous " cure. " Materials and Methods We reviewed the radiographic and medical records of eight consecutive patients studied at our hospital in 1977 who had an angiographic diagnosis of carotid- cavernous sinus Received September 24, 1979; accepted after fistula. -
Dural Venous Channels: Hidden in Plain Sight–Reassessment of an Under-Recognized Entity
Published July 16, 2020 as 10.3174/ajnr.A6647 ORIGINAL RESEARCH INTERVENTIONAL Dural Venous Channels: Hidden in Plain Sight–Reassessment of an Under-Recognized Entity M. Shapiro, K. Srivatanakul, E. Raz, M. Litao, E. Nossek, and P.K. Nelson ABSTRACT BACKGROUND AND PURPOSE: Tentorial sinus venous channels within the tentorium cerebelli connecting various cerebellar and su- pratentorial veins, as well as the basal vein, to adjacent venous sinuses are a well-recognized entity. Also well-known are “dural lakes” at the vertex. However, the presence of similar channels in the supratentorial dura, serving as recipients of the Labbe, super- ficial temporal, and lateral and medial parieto-occipital veins, among others, appears to be underappreciated. Also under-recog- nized is the possible role of these channels in the angioarchitecture of certain high-grade dural fistulas. MATERIALS AND METHODS: A retrospective review of 100 consecutive angiographic studies was performed following identification of index cases to gather data on the angiographic and cross-sectional appearance, location, length, and other features. A review of 100 consecutive dural fistulas was also performed to identify those not directly involving a venous sinus. RESULTS: Supratentorial dural venous channels were found in 26% of angiograms. They have the same appearance as those in the tentorium cerebelli, a flattened, ovalized morphology owing to their course between 2 layers of the dura, in contradistinction to a rounded cross-section of cortical and bridging veins. They are best appreciated on angiography and volumetric postcontrast T1- weighted images. Ten dural fistulas not directly involving a venous sinus were identified, 6 tentorium cerebelli and 4 supratentorial. -
CT Observations Pertinent to Septic Cavernous Sinus Thrombosis
755 CT Observations Pertinent to Septic Cavernous Sinus Thrombosis Jamshid Ahmadi1 The use of high-resolution computed tomography (CT) is described in four patients James R. Keane2 with septic cavernous sinus thrombosis, In all patients CT findings included multiple Hervey D. Segall1 irregular filling defects in the enhancing cavernous sinus. Unilateral or bilateral inflam Chi-Shing Zee 1 matory changes in the orbital soft tissues were also present. Enlargement of the superior ophthalmic vein due to extension of thrombophlebitis was noted in three patients. Since the introduction of antibiotics, septic cavernous sinus thrombosis (throm bophlebitis) has become a rare disease [1-4]. Despite considerable improvement in morbidity and mortality (previously almost universal), it remains a potentially lethal disease. The diagnosis of cavernous sinus thrombophlebitis requires a careful clinical evaluation supplemented with appropriate laboratory and radiographic studies. Current computed tomographic (CT) scanners (having higher spatial and contrast resolution) play an important role in the radiographic evaluation of the diverse pathologiC processes that involve the cavernous sinus [5-7]. The use of CT has been documented in several isolated cases [8-13], and small series [14] dealing with the diagnosis and management of cavernous sinus thrombophlebitis. CT scanning in these cases was reported to be normal in two instances [8 , 10]. In other cases so studied, CT showed abnormalities such as orbital changes [11 , 14], paranasal sinusitis [12], and associated manifestations of intracranial infection [9]; however, no mention was made in these cases of thrombosis within the cavernous sinus itself. Direct CT demonstration of thrombosis within the cavernous sinus has been rarely reported [13]. -
Varicose Veins and Superficial Thrombophlebitis
ENTITLEMENT ELIGIBILITY GUIDELINES VARICOSE VEINS AND SUPERFICIAL THROMBOPHLEBITIS 1. VARICOSE VEINS MPC 00727 ICD-9 454 DEFINITION Varicose Veins of the lower extremities are a dilatation, lengthening and tortuosity of a subcutaneous superficial vein or veins of the lower extremity such as the saphenous veins and perforating veins. A diagnosis of varicose veins is sometimes made in error when the veins are prominent but neither varicose or abnormal. This guideline excludes Deep Vein Thrombosis, and telangiectasis. DIAGNOSTIC STANDARD Diagnosis by a qualified medical practitioner is required. ANATOMY AND PHYSIOLOGY The venous system of the lower extremities consists of: 1. The deep system of veins. 2. The superficial veins’ system. 3. The communicating (or perforating) veins which connect the first two systems. There are primary and secondary causes of varicose veins. Primary causes are congenital and/or may develop from inherited conditions. Secondary causes generally result from factors other than congenital factors. VETERANS AFFAIRS CANADA FEBRUARY 2005 Entitlement Eligibility Guidelines - VARICOSE VEINS/SUPERFICIAL THROMBOPHLEBITIS Page 2 CLINICAL FEATURES Clinical onset usually takes place when varicosities in the affected leg or legs appear. Varicosities typically present as a bluish discolouration and may have a raised appearance. The affected limb may also demonstrate the following: • Aching • Discolouration • Inflammation • Swelling • Heaviness • Cramps Varicose Veins may be large and apparent or quite small and barely discernible. Aggravation for the purposes of Varicose Veins may be represented by the veins permanently becoming larger or more extensive, or a need for operative intervention, or the development of Superficial Thrombophlebitis. PENSION CONSIDERATIONS A. CAUSES AND/OR AGGRAVATION THE TIMELINES CITED BELOW ARE NOT BINDING. -
Chapter 23 PARANASAL SINUS FRACTURES
Paranasal Sinus Fractures Chapter 23 PARANASAL SINUS FRACTURES † MARK GIBBONS, MD, FACS,* AND NATHAN SALINAS, MD INTRODUCTION ANATOMY DIAGNOSIS: CLINICAL AND IMAGING STUDIES MANAGEMENT ISSUES AND ALGORITHM SUMMARY CASE PRESENTATIONS Case Study 23-1 Case Study 23-2 *Lieutenant Colonel (Retired), Medical Corps, US Army; formerly, Chief, Department of Otolaryngology, Carl R. Darnall Army Medical Center, 36000 Darnall Loop, Fort Hood, Texas 76544 †Major, Medical Corps, US Army; Chief, Department of Otolaryngology, Fort Wainwright, 4076 Neely Road, Fort Wainwright, Alaska 99703 281 Otolaryngology/Head and Neck Combat Casualty Care INTRODUCTION Frontal sinus trauma may be blunt or penetrating, combat injuries, nearly half of all patients with both with frontal sinus fractures representing 6% to 12% of cranial and ocular combat injuries requiring surgical craniofacial fractures.1,2 Two-thirds of patients with intervention also underwent frontal sinus repair, frontal sinus trauma may have sustained concomitant obliteration, or cranialization.8 Another contempo- injuries to other facial structures.3 Contemporary al- rary review of facial trauma following improvised gorithms for classification and management of frontal explosive device blasts identified trauma to the sinus trauma are largely based on civilian injury pat- forehead aesthetic subunit as a “danger zone” in terns, which carry a trend toward high-velocity blunt massive facial trauma, which was defined as injury trauma.1,2,4,5 to three or more facial units.9 Because massive facial War