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\vskip16pt \textcolor{GJBlue}{\large\bfseries\abstractname\space} }{% \vskip8pt \textcolor{GJMediumGrey}{\rule{\textwidth}{2pt}} \vskip16pt } \usepackage[absolute,overlay]{textpos} \makeatother \usepackage{lineno} \linenumbers \begin{document} \author[1]{Marian Fayek Farid Kolta} \author[2]{Youssriah Yahia Sabri} \affil[1]{ Cairo University Hospitals} \renewcommand\Authands{ and } \date{\small \em Received: 8 December 2013 Accepted: 4 January 2014 Published: 15 January 2014} \maketitle \begin{abstract} The superior vena cava (SVC) syndrome is a clinical entity caused by obstruction of the superior vena cava by infiltration, compression or thrombosis. Cancer is the most common underlying cause of superior vena cava obstruction. The incidence of catheter-induced superior vena cava obstruction is rapidly increasing. Fibrosing mediastinitis and Behçet disease are rare causes of SVC syndrome. Clinical presentation of SVC syndrome may include cough, dyspnea, dysphagia, and swelling or discoloration of the neck, face and upper extremities. Aim of this study is to evaluate the role of Multislice CT in study of superior vena cava obstruction syndromes and assessment of collateral circulation in different causes of superior vena caval obstruction \end{abstract} \keywords{} \begin{textblock*}{18cm}(1cm,1cm) % {block width} (coords) \textcolor{GJBlue}{\LARGE Global Journals \LaTeX\ JournalKaleidoscope\texttrademark} \end{textblock*} \begin{textblock*}{18cm}(1.4cm,1.5cm) % {block width} (coords) \textcolor{GJBlue}{\footnotesize \\ Artificial Intelligence formulated this projection for compatibility purposes from the original article published at Global Journals. However, this technology is currently in beta. \emph{Therefore, kindly ignore odd layouts, missed formulae, text, tables, or figures.}} \end{textblock*} \let\tabcellsep& \section[{Introduction}]{Introduction}\par he superior vena cava (SVC) syndrome is a clinical entity caused by obstruction of the superior vena cava by infiltration, compression or thrombosis. Although clinical symptoms of the disorder were first described in 1757 in a patient with a syphilitic aneurysm of the ascending aorta, vascular causes are now rare and approximately 90\% of cases are associated with a cancerous tumor that is compressing the superior vena cava, such as bronchogenic carcinoma including small cell and non-small cell lung carcinoma, Burkitt's lymphoma, lymphoblastic lymphomas, acute lymphoblastic leukemia (rare), and other acute leukemias (Krimsky et al, 2002). Tuberculosis has also been known to cause superior vena cava syndrome (SVCS). SVCS can be caused by invasion or compression by a pathological process or by thrombosis in the vein itself, although this latter is less common (approximately 35\% due to the use of Benign Causes of Superior Vena Cava Obstruction Iatrogenic superior vena cava obstructionthe incidence of catheter-induced superior vena cava obstruction is rapidly increasing e.g. large central venous catheters, such as dialysis catheters, Hickman catheters, and parenteral nutrition catheters \hyperref[b2]{(3)}. Fibrosing mediastinitis is a rare histologically benign disorder caused by proliferation of collagen tissue and fibrosis in the mediastinum \hyperref[b3]{(4)}. Behçet disease is a rare systemic disease in which superior vena cava stenosis or occlusion may result (5).\par Clinical presentation of SVC syndrome: SVC syndrome is caused by gradual compression of the SVC, leading to edema and retrograde flow, but it can also be caused more abruptly in thrombotic cases. Symptoms may include cough, dyspnea, dysphagia, and swelling or discoloration of the neck, face and upper extremities. Often, collateral venous circulation causes distension of the superficial veins in the chest wall. Although SVC syndrome is usually a clinical diagnosis, plain radiography, computed tomography (CT) and venography are used for confirmation. (6).\par CT Findings: CT can diagnose SVC affection in SVC syndrome and can detect subclinical superior vena cava obstruction in patients who are relatively asymptomatic (Yu JB et al, 2008). Regardless of its cause, the CT diagnosis of superior vena cava obstruction includes lack of opacification of the superior vena cava, an intraluminal filling defect or severe narrowing of the superior vena cava, and visualization of collateral vascular channels {\ref (Eren et al, 2006}). MDCT, with its multiplanar and 3D imaging capabilities, allows thorough anatomic delineation of the various collateral pathways diverting the blood from the site of obstruction. Although axial images allow evaluation of potential causes of superior vena cava obstruction, such as a mediastinal mass, MDCT provides information about the level and degree of superior vena cava obstruction, the length of the affected segment, and the presence or absence of intraluminal clot distal to the obstruction, thereby allowing the interventional radiologist to choose the optimal treatment option. {\ref (Plekker et al, 2008)}. \section[{II.}]{II.} \section[{Aim of the work}]{Aim of the work} \section[{Patients and methods}]{Patients and methods} \section[{a) Patients}]{a) Patients}\par This study involved 20 patients; 13 males and 7 females, age range 15-69 (average of 39.3years). Cases were referred from the chest department to the radiology department in Kasr Al-Aini for MSCT of the chest.\par Twelve patients presented clinically with mediastinal syndrome; of whom six cases were biopsy proved central Bronchogenic carcinoma, five were known cases of Behçet disease and one case with unknown etiology.\par Two cases had right upper limb DVT. Two cases had lymphoma and one case was surveyed for chest metastases. One case had fever of unknown origin after chemotherapy. One case with antiphospholipid antibody syndrome where echo detected calcified right atrial thrombus. One case with bilateral pleural effusion. (See table \hyperref[tab_1]{1}). \section[{Results}]{Results}\par See the summary of MSCT results in tables 2-4. \section[{Discussion}]{Discussion}\par Multi-detector row computed tomography (CT) with 2D and 3D reconstructed images provides a unique perspective on thoracic anatomy and disease. Multidetector row CT allows shorter acquisition times, greater coverage, and superior image resolution \hyperref[b4]{(7)}.\par In vascular imaging, this would provide image quality that equals or surpasses that of conventional angiography. Its use has expanded to aid in diagnosis and surgical planning, as it is reliable in depicting clot, thoracic vasculature and may also be used to evaluate thoracic venous anomalies and to plan therapy \hyperref[b5]{(8)}.\par Multi-detector row CT has been used for venous angiography. Superior vena cava obstruction, often related to tumor, is frequently seen at multidetector row CT. This technique may be used to establish the extent of tumor involvement and document the extent of collateral vessel formation \hyperref[b6]{(9)}.\par MDCT, with its multi-planar imaging capabilities, allows thorough anatomic delineation of the various collateral pathways diverting the blood from the site of obstruction. Although axial images allow evaluation of potential causes of superior vena cava obstruction, such as a mediastinal mass, if intervention is warranted, MDCT provides valuable information about the level and egree of superior vena cava obstruction, the length of the affected segment, and the presence or absence of intra-luminal clot distal to the obstruction, thereby allowing the interventional radiologist to choose the optimal treatment option \hyperref[b7]{(10)}.\par Superior vena cava syndrome usually presents more gradually with an increase in symptoms over time as malignancies increase in size or invasiveness \hyperref[b8]{(11)}.\par The severity of the syndrome depends on the rapidity of onset of the obstruction and its location \hyperref[b10]{(12)}. (see table \hyperref[tab_6]{5}). SVC syndrome can lead to the formation of downhill esophageal varices and pleural effusion. Numerous case reports have described pleural effusions in conjunction with the SVC syndrome. These effusions occur in 60\% of SVC syndrome cases. The effusions are small, usually occupying less than one-half of the affected hemithorax, and occur approximately equally on either side or bilaterally. Although previously thought to be largely transudates, a large case series found that 18\% of the effusions were chylous, with the remainder being exudates. None of the effusions sampled in the series were transudates. Occluded lymphatic flow from increased hydrostatic pressure in the SVC and left brachiocephalic vein probably contributes to the development of chylous pleural fluid. The pathophysiology of the exudative effusions, however, remains unknown. Many factors, including diuresis, small pulmonary emboli, and the underlying inflammatory or malignant condition all likely contribute. Chylous or exudative pleural effusions occur in most patients with SVC syndrome. The effusions are usually small and resolve upon correction of the underlying SVC obstruction. ( (13).\par Five to 10 percent of cases of SVC obstruction are due to benign causes. Most result from invasive monitoring techniques, such as the placement of central venous lines, Swan-Ganz catheters, and interventional techniques, such as the placement of pacemakers and central venous catheters for chemotherapy \hyperref[b13]{(14)}. Thrombi in the SVC were detected by transesophageal echocardiography in 30\% of patients who had single lumen silicone rubber hemo-dialysis catheters. Polyvinyl chloride, polyethylene and teflon catheters are associated with increased thrombogenisity, as compared to silicone rubber. Furthermore, the SVC stenosis may be induced by persistent trauma of the endothelium by the catheter tip and the higher blood flow during dialysis hours ( \hyperref[b16]{(17)}.\par Fibrosing mediastinitis (fig {\ref 5})-it is a rare benign disorder caused by proliferation of acellular collagen and fibrous tissue within the mediastinum. Although many cases are idiopathic, many (and perhaps most) cases in the United States are thought to be caused by an abnormal immunologic response to Histoplasma capsulatum infection. Affected patients are typically young and present with signs and symptoms of obstruction or compression of the superior vena cava, pulmonary veins or arteries, central airways, or esophagus. There may be two types of fibrosing mediastinitis: focal and diffuse. The focal type usually manifests on computed tomographic (CT) or magnetic resonance (MR) images as a localized, calcified mass in the paratracheal or sub-carinal regions of the mediastinum or in the pulmonary hila. The diffuse type manifests on CT or MR images as a diffusely infiltrating, often non-calcified mass that affects multiple mediastinal compartments. CT and MR imaging play a vital role in the diagnosis and management of fibrosing mediastinitis \hyperref[b17]{(18)}.\par Behçet disease (fig 6,7) -Behçet disease is a multisystem disease of unknown etiology. The syndrome carries the name of the Turkish dermatologist Hulusi Behçet, who, in 1937, described a syndrome of recurrent aphthous ulcers, genital ulcerations, and uveitis leading to blindness. Although the cause of the disease is still unknown, it has become recognized as a multisystemic inflammatory disease \hyperref[b18]{(19)}. Enlargement of the thyroid gland (goiter) \hyperref[b19]{(20)}. The aim of this study was to provide evidence that MSCT is useful in patients with superior vena caval obstruction, detecting the level and the cause of obstruction.\par Multi-slice CT scans were reviewed in 20 patients referred from chest department to radiology department in Kasr Al-Aini.\par Twelve patients presented clinically in our study with mediastinal syndrome, Two cases had right upper limb DVT. Two cases had lymphoma and one case was surveyed for chest metastases. One case had fever of unknown origin after chemotherapy. One case with antiphospholipid antibody syndrome where echo detected calcified right atrial thrombus. One case with bilateral pleural effusion\par The twelve patients presented clinically in our study with mediastinal syndrome, six cases were biopsy proved central Bronchogenic carcinoma, five were known cases of Behçet disease and one case with unknown etiology. These findings are more or less consistent with the study made by Bagheri et al, 2009 which stated that among 45 patients with SVCS, their diagnostic pathological reports showed 26 (57.8\%) were compatible with bronchogenic carcinoma (small cell lung cancer [SCLC] in 19 cases and non-SCLC in 7) which was the most common etiology of superior vena cava syndrome. Lymphoma was reported in 14 cases (31.1\%), (12 of non-Hodjkin's lymphoma and 2 of Hodjkin's lymphoma), and germ cell tumor and malignant thymoma were observed in 3 (6.7\%) and 2 (4.4\%) of patients \hyperref[b20]{(21)}. In our study, 5 Behçet cases revealed partial SVC obstruction and eminent mediastinal collaterals, 6 cases with central infiltrating Bronchogenic carcinoma revealed partially infiltrated SVC with few collaterals noted in 5 cases and eminent chest wall collaterals in one case (the case was a follow up case of Bronchogenic carcinoma after radiotherapy), 1 Case of mediastinal syndrome of unknown etiology showed diffuse affection of the mediastinum with soft tissue density lesion causing effacement of SVC and marked attenuation of the right pulmonary artery ; a picture suggesting fibrosing mediastinitis with eminent chest wall collaterals, 2 cases with left upper limb DVT seen extending into left brachiocephalic vein and normal contra-lateral brachiocephalic vein and SVC, 2 cases with lymphoma showed huge anterior mediastinal mass, displaced and compressed SVC with no collaterals, one case of chest assessment for metastasis revealed lung, pleura and mediastinal metastases with SVC distortion and partial infiltration and no collaterals, one case of fever of unknown origin after chemotherapy showed partial SVC obstruction with a heterogenous thrombus with air density, enlarged SVC, no collaterals, one case of Antiphospholipid antibody syndrome revealed partial SVC obstruction at lowest portion , no collaterals, one case of bilateral pleural effusion revealed partial SVC thrombus in relation to CV-Line catheter, no collaterals.\par To conclude, the rate of obstruction and its location greatly affects the severity of symptoms of SVCS, this depends on the development of the collateral circulation. Meaning that when the onset of obstruction is slow (as in benign causes of obstruction e.g. Behcet's disease and with central venous catheters), the collateral circulation will have time to distend and accommodate the increased blood flow. On the other hand, diseases causing rapid onset of obstruction (malignant tumors), produce more severe symptoms because the collateral veins will not have time to distend. L Longmore et al, 2007 suggested that the general recruitment of venous collaterals over time may lead to remission of the syndrome although the SVC remains obstructed \hyperref[b23]{(24)}.\par Wilson, 2007 stated that not all cases of SVC obstruction must present with SVCS (e.g. facial edema, venous distension in the neck, upper limb edema) and that there is 10\% of cases may have radiographic SVC obstruction in absence of symptoms. This is consistent with our study which includes twelve of the twenty patients presented clinically with mediastinal syndrome, two cases had right upper limb DVT, two cases had lymphoma and one case was surveyed for chest metastasis. One case had fever of unknown origin after chemotherapy, one case with anti-phospholipid antibody syndrome and one case with bilateral pleural effusion (25).\par VI. \section[{Summary and Conclusion}]{Summary and Conclusion}\par Superior vena cave syndrome (SCVS) is a constellation of signs and symptoms resulting from obstruction of the SVC or its major tributaries by intraluminal occlusion or by extrinsic compression and/or invasion from malignant and benign diseases.\par SVC obstruction leads to increased venous pressure and edema of the neck, arms, upper chest, and head causing increased intracranial pressure. Patient may present with headache, syncope or presyncope, nausea and vomiting, hoarseness, dysphagia, cough, dyspnea and chest pain. Severity of symptoms depend on the time course of obstruction. As obstruction develops, venous collaterals develop to find alternate pathways for venous return to the right atrium. In the post-antibiotic era malignancy remains the commonest etiology. Lung cancer is the commonest malignancy. SVCS is most common with small cell lung cancer as it grows rapidly in central airways. CT chest is the investigation of choice which provides information on location, possible etiology, extent of collaterals and guide biopsy attempts.\par The advent of multi-detector CT has revolutionized imaging of the mediastinal vascular structures. In comparison to single-detector helical CT scanners, multi-detector scanners not only provide faster speed, greater coverage, and improved spatial resolution, but also have the unique ability to create images of thick and thin collimation from the same data set.\par One of the greatest benefits of this new technology is the improved quality of two-dimensional (2D) multi-planar and three-dimensional (3D) reconstruction images.\par MSCT can easily prove or exclude the affection of SVC by partial or complete obstruction, the development of collateral circulation as well as detecting the cause of obstruction whether thrombosis, compression or infiltration and its extent. \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-2.png} \caption{\label{fig_0}}\end{figure} \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-3.png} \caption{\label{fig_1}}\end{figure} \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-4.png} \caption{\label{fig_2}}\end{figure} \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-5.png} \caption{\label{fig_3}}\end{figure} \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-6.png} \caption{\label{fig_4}}\end{figure} \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-7.png} \caption{\label{figure7}}\end{figure} \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-8.png} \caption{\label{figure8}}\end{figure} \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-9.png} \caption{\label{figure9}}\end{figure} \begin{figure}[htbp] \noindent\textbf{1} \par \begin{longtable}{P{0.7313669064748202\textwidth}P{0.10884892086330934\textwidth}P{0.009784172661870504\textwidth}} \multicolumn{2}{l}{Showing patients' presentation}\\ R Referred case\tabcellsep \multicolumn{2}{l}{Number of patients}\\ Mediastinal syndrome\tabcellsep \tabcellsep 12\\ Upper limb DVT\tabcellsep \tabcellsep 2\\ \multicolumn{2}{l}{Chest assessment in case of lymphoma}\tabcellsep 2\\ Chest assessment for metastases\tabcellsep \tabcellsep 1\\ \multicolumn{2}{l}{Fever of unknown origin after chemotherapy}\tabcellsep 1\\ Antiphospholipid antibody syndrome\tabcellsep \tabcellsep 1\\ Bilateral pleural effusion\tabcellsep \tabcellsep 1\\ b) Methods\tabcellsep \multicolumn{2}{l}{administration of 40 ml of omnipaque 350 mg/ml at}\\ All patients were subjected to:\tabcellsep a rate of 3 ml/sec.\\ 1. Thorough clinical examination with history taking, general and chest examination.\tabcellsep \multicolumn{2}{l}{IV.}\\ 2. Routine laboratory tests mostly complete blood\tabcellsep \\ picture, other tests were considered according to\tabcellsep \\ case e.g. culture and sensitivity.\tabcellsep \\ 3. MSCT of the chest: Toshiba Aquilion MSCT 64\tabcellsep \\ channels was used. All cases were given pump IV\tabcellsep \end{longtable} \par \caption{\label{tab_1}Table 1 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{2} \par \begin{longtable}{P{0.85\textwidth}} shows summary of the MSCT findings in our 20\\ cases, while table 3 gives summary of the SVC different\\ MSCT appearances and table 4 shows collateral\\ circulation in MSCT.\end{longtable} \par \caption{\label{tab_2}Table 2}\end{figure} \begin{figure}[htbp] \noindent\textbf{2} \par \begin{longtable}{P{0.2155141843971631\textwidth}P{0.6344858156028369\textwidth}} \tabcellsep 1\\ \tabcellsep 1\\ \tabcellsep 1 1\\ \tabcellsep 1 1\\ \tabcellsep ni ni\\ \tabcellsep IV.\\ d\tabcellsep u\\ \tabcellsep bl bl\\ \tabcellsep p\\ gi\tabcellsep at\\ Case presentation ation\tabcellsep MSCT finding\\ 5 Behçet cases\tabcellsep -Partial SVC obstruction\\ \tabcellsep -Eminent mediastinal collaterals\\ 6 central infiltrating Bronchogenic carcinoma\tabcellsep Partially Infiltrated SVC with few collaterals noted in 5 cases and\\ \tabcellsep eminent c chest wall collaterals in one case (the case was a\\ \tabcellsep follow up case of Bronchogenic carcinoma after radiotherapy).\\ Case of mediastinal syndrome of unknown etiology un\tabcellsep Diffuse affection of the mediastinum with soft tissue density\\ \tabcellsep lesion causing effacement of SVC and marked attenuation of\\ \tabcellsep the right pulmonary artery ; a picture suggesting fibrosing\\ \tabcellsep mediastinitis*\\ \tabcellsep Eminent c chest wall collaterals seen.\\ 2 cases with left upper limb DVT\tabcellsep DVT seen extending into left brachiocephalic vein. Normal\\ \tabcellsep contralateral brachiocephalic vein and SVC.\\ 2 cases with lymphoma\tabcellsep Huge anterior mediastinal mass .Displaced and compressed\\ \tabcellsep SVC.\\ \tabcellsep No collaterals\\ One case of chest assessment for metastases\tabcellsep Lung, pleura and mediastinal metastases .SVC distortion and\\ \tabcellsep partial infiltration .\\ \tabcellsep No collaterals\\ One case of fever of unknown origin after chemotherapy\tabcellsep Partial SVC obstruction with a heterogenous thrombus**with air\end{longtable} \par {\small\itshape [Note: density, enlarged SVC, no collaterals One case of Antiphospholipid antibody syndrome Partial SVC obstruction at lowest portion , no collaterals One case of bilateral pleural effusion Partial SVC thrombus in relation to CV-Line catheter, no collaterals *case was proved fibrosing mediastinitis. ** Case was proved to have MRSA infection.]} \caption{\label{tab_3}Table 2 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{2le3} \par \begin{longtable}{P{0.5348314606741573\textwidth}P{0.3151685393258427\textwidth}} M MSCT SVC findings\tabcellsep No. of cases\\ Partial obstruction\tabcellsep 9 cases\\ Infiltration\tabcellsep 7 cases\\ Normal\tabcellsep 4 cases\end{longtable} \par \caption{\label{tab_4}Table 2 : le Table 3 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{4} \par \begin{longtable}{P{0.5647651006711409\textwidth}P{0.2852348993288591\textwidth}} No of cases\tabcellsep HRCT finding\\ 5 Behçet cases\tabcellsep Eminent collaterals\\ 1 case of fibrosing mediastinitis\tabcellsep Eminent collaterals\\ 1 case of infected thrombus\tabcellsep No collaterals\\ 2 cases with partial thrombus\tabcellsep No collaterals\\ 5 cases of malignant mediastinal\tabcellsep Few collaterals mostly chest\\ infiltration by Bronchogenic carcinoma\tabcellsep \\ 1 case of follow up Bronchogenic\tabcellsep Eminent chest wall collaterals\\ carcinoma with SVC infiltration\tabcellsep \\ 1 case of 2ry malignant mediastinal\tabcellsep No collaterals\\ infiltration.\tabcellsep \\ V.\tabcellsep \end{longtable} \par \caption{\label{tab_5}Table 4 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{5} \par \begin{longtable}{P{0.011402439024390244\textwidth}P{0.07567073170731707\textwidth}P{0.021768292682926828\textwidth}P{0.030060975609756093\textwidth}P{0.6489024390243903\textwidth}P{0.008292682926829269\textwidth}P{0.044573170731707315\textwidth}P{0.009329268292682926\textwidth}} \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep Year 2014\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep T,\tabcellsep s m -\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep or\tabcellsep h a\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep ath\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep ru ru\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep e\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep ge e\tabcellsep \tabcellsep ov\\ \tabcellsep \tabcellsep \tabcellsep ti\tabcellsep s\tabcellsep -\tabcellsep t\tabcellsep l\\ \tabcellsep n\tabcellsep her\tabcellsep l l n used ( . .\tabcellsep m\tabcellsep ma\tabcellsep ( D D D D ) D\\ \tabcellsep h\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\ \tabcellsep or i or\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\ \tabcellsep el el\tabcellsep (9) ).\tabcellsep \tabcellsep \tabcellsep \\ Grade\tabcellsep Category\tabcellsep \multicolumn{2}{l}{Incidence \%}\tabcellsep \tabcellsep \tabcellsep Definition\\ 0\tabcellsep Asymptomatic\tabcellsep \tabcellsep 10\tabcellsep \multicolumn{3}{l}{Radiographic superior vena cava obstruction in the absence}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{2}{l}{of symptoms}\\ 1\tabcellsep Mild\tabcellsep \tabcellsep 25\tabcellsep \multicolumn{3}{l}{Edema in head or neck (vascular distention), cyanosis,}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{2}{l}{plethora}\\ 2\tabcellsep Moderate\tabcellsep \tabcellsep 50\tabcellsep \multicolumn{3}{l}{Edema in head or neck with functional impairment (mild}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{3}{l}{dysphagia, cough, mild or moderate impairment of head, jaw}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{3}{l}{or eyelid movements, visual disturbances caused by ocular}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep edema)\tabcellsep \\ 3\tabcellsep Severe\tabcellsep \tabcellsep 10\tabcellsep \multicolumn{3}{l}{Mild or moderate cerebral edema (headache, dizziness) or}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{3}{l}{mild/moderate laryngeal edema or diminished cardiac reserve}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{3}{l}{(syncope after bending)}\\ 4\tabcellsep Life-threatening\tabcellsep \tabcellsep 5\tabcellsep \multicolumn{3}{l}{Significant cerebral edema (confusion, obtundation) or}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{3}{l}{significant laryngeal edema (stridor) or significant}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{3}{l}{hemodynamic compromise (syncope, hypotension, renal}\\ \tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{2}{l}{insufficiency)}\\ 5\tabcellsep Fatal\tabcellsep \tabcellsep <1\tabcellsep Death\tabcellsep \end{longtable} \par \caption{\label{tab_6}Table 5 :}\end{figure} \footnote{© 2014 Global Journals Inc. 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