DOCSLIB.ORG

Chronic Thromboembolic Pulmonary Hypertension (CTEPH)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Chronic Thromboembolic Pulmonary Hypertension (CTEPH) medicina Review Revisiting a Distinct Entity in Pulmonary Vascular Disease: Chronic Thromboembolic Pulmonary Hypertension (CTEPH) Munish Sharma 1 and Deborah Jo Levine 2,* 1 Corpus Christi Medical Center, Department of Pulmonary Medicine, Corpus Christi, TX 78412, USA; [email protected] 2 Department of Pulmonary Medicine, University of Texas Health Science Center, San Antonio, TX 78229, USA * Correspondence: [email protected] Abstract: Chronic thromboembolic pulmonary hypertension (CTEPH) is a specific type of pulmonary hypertension (PH) and the major component of Group 4 pulmonary hypertension (PH). It is caused by pulmonary vasculature obstruction that leads to a progressive increase in pulmonary vascular resistance and, ultimately, to failure of the right ventricle. Pulmonary thromboendarterectomy (PEA) is the only definitive therapy, so a timely diagnosis and early referral to a specialized PEA center to determine candidacy is prudent for a favorable outcome. Percutaneous balloon pulmonary angioplasty (BPA) has a potential role in patients unsuitable for PEA. Medical therapy with riociguat is the only PH-specific medical therapy currently approved for the treatment of inoperable or persistent CTEPH. This review article aims to revisit CTEPH succinctly with a review of prevailing literature. Keywords: chronic thromboembolic pulmonary hypertension; pulmonary embolism; pulmonary thromboendarterectomy; percutaneous balloon pulmonary angioplasty; riociguat; ventilation-perfusion lung scan; computed tomography pulmonary angiography; pulmonary angiography Citation: Sharma, M.; Levine, D.J. Revisiting a Distinct Entity in Pulmonary Vascular Disease: Chronic Thromboembolic Pulmonary 1. Introduction Hypertension (CTEPH). Medicina The 6th world symposium on pulmonary hypertension (PH) in 2018 has defined PH 2021, 57, 355. https://doi.org/ as an elevated mean pulmonary artery pressure (mPAP) ≥ 20 mmHg at rest, pulmonary 10.3390/medicina57040355 capillary wedge pressure < 15 mmHg, and pulmonary vascular resistance (PVR) ≥ 3 Wood Unit (WU) [1]. PH can be further subdivided into 5 groups (Table1). Academic Editor: Camelia Diaconu Table 1. Different groups of pulmonary hypertension. Left column indicates group of pulmonary Received: 10 February 2021 hypertension and right column shows the entity included. Accepted: 2 April 2021 Published: 7 April 2021 Group 1 Pulmonary Arterial Hypertension (PAH) Group 2 Due to Left Heart Disease Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in Group 3 Due to Chronic Lung Disease/Hypoxemia published maps and institutional affil- Group 4 Due to Pulmonary Arterial Obstructions iations. Group 5 Multifactorial Chronic thromboembolic pulmonary hypertension (CTEPH) belongs to Group 4 of the PH classification. CTEPH is defined as an obstruction of the pulmonary arterial vasculature Copyright: © 2021 by the authors. secondary to single or recurrent episodes of pulmonary embolism (PE) [2]. It is a distinct Licensee MDPI, Basel, Switzerland. This article is an open access article and infrequently diagnosed entity of PH that is progressive and can be fatal if left untreated. distributed under the terms and 2. Epidemiology conditions of the Creative Commons Attribution (CC BY) license (https:// CTEPH occurs in a minority of the patients who fail to restore normal pulmonary creativecommons.org/licenses/by/ perfusion after single or recurrent episodes of PE. It generally develops within the first 4.0/). year after PE and is an uncommon occurrence after about 2 years of an episode of PE [2]. Medicina 2021, 57, 355. https://doi.org/10.3390/medicina57040355 https://www.mdpi.com/journal/medicina Medicina 2021, 57, 355 2 of 12 The exact incidence of CTEPH is difficult to determine but it is estimated to be prevalent in around 0.5–5% of patients that have an acute PE [3–6]. It has been reported in as many as 11.6% of patients with a history of recurrent PE [7] (Table2). Table 2. Studies estimating incidences of chronic thromboembolic pulmonary (CTEPH) after pulmonary embolism (PE). Investigators Year of Publication Type of Study Main Results -CTEPH incidence was 3.2% (95% CI 2–4.4) of 999 patients who survived after PE ≥ 2 years (4 studies) Metanalysis of patients with PE followed up for CTEPH. Ende-Verhaar YM et al. [3] February 2017 -Pooled CTEPH incidence 0.56% Sample size n: 4047 patients (95% CI 0.1–1.0) (3 studies) from 16 studies -In survivors without major comorbidities, incidence was 2.8% in 1775 patients (9 studies) Prospective study of 320 patients with proven PE 4 out of 320 patients with proven Miniati M et al. [4] September 2006 follow-up for a median PE (1%) developed CTEPH duration of 2.1 years Cohort screening study in 866 CTEPH incidence was 0.57% (95% patients with acute PE studied CI, 0.02–1.2%) in all-cause PE and Klok FA et al. [5] January 2010 between January 2001 and 1.5% (95% CI, 0.08–3.1%) in July 2007 provoked PE Prospective follow-up of 223 patients with acute PE for median duration of 94.3 CTEPH incidence was 1% (95% months. Follow-up CI, 0.0–2.4) at 6 months, 3.1% Pengo V. [6] May 2004 ventilation-perfusion scan and (95% CI, 0.7–5.5) at 1 year, and pulmonary angiography done 3.8% (95 CI, 1.1–6.5) at 2 years in patients suspected to have CTEPH Cohort screening study of CTEPH in 5 patients (11.6%) Berghaus TM [7] December 2011 43 survivors of recurrent PE patients with recurrent PE Determining an accurate incidence of CTEPH after PE is challenging because of inconsistencies in reporting. An international registry for CTEPH from North America and Europe reported that up to 75% of patients with CTEPH had a definite proceeding episode of PE [8]. In contrast, data from Japan reported antecedent PE in around 15–33% of patients with CTEPH [9,10]. Studies from Japan have shown 80% female preponderance, while those from North America and Europe have reported around 49.9% incidence in females [8,9]. The nonspecific presentation of the disease, underutilization of the guideline- recommended ventilation-perfusion (V/Q) scan for screening, and lack of expertise in interpreting nuclear and radiological studies have made it difficult to quantify the burden of CTEPH more uniformly across the world. 3. Pathophysiology of CTEPH The current understanding of the pathophysiology of CTEPH indicates a more com- plex phenomenon than mere chronic obstruction of pulmonary vascular bed by unresolved thrombus and subsequent right ventricular (RV) dysfunction. Chronic obstruction of proximal pulmonary vessels by fibrotic clots, development of small vessel disease, and progressive diffuse remodeling of the pulmonary vasculature collectively represent the pathophysiology of CTEPH [10,11]. Medicina 2021, 57, x FOR PEER REVIEW 3 of 13 ventilation-perfusion scan year, and 3.8% (95 CI, 1.1– and pulmonary angiography 6.5) at 2 years done in patients suspected to have CTEPH Cohort screening study of 43 CTEPH in 5 patients (11.6%) Berghaus TM [7] December 2011 survivors of recurrent PE patients with recurrent PE Determining an accurate incidence of CTEPH after PE is challenging because of in- consistencies in reporting. An international registry for CTEPH from North America and Europe reported that up to 75% of patients with CTEPH had a definite proceeding episode of PE [8]. In contrast, data from Japan reported antecedent PE in around 15–33% of pa- tients with CTEPH [9,10]. Studies from Japan have shown 80% female preponderance, while those from North America and Europe have reported around 49.9% incidence in females [8,9]. The nonspecific presentation of the disease, underutilization of the guide- line-recommended ventilation-perfusion (V/Q) scan for screening, and lack of expertise in interpreting nuclear and radiological studies have made it difficult to quantify the burden of CTEPH more uniformly across the world. 3. Pathophysiology of CTEPH The current understanding of the pathophysiology of CTEPH indicates a more com- plex phenomenon than mere chronic obstruction of pulmonary vascular bed by unre- solved thrombus and subsequent right ventricular (RV) dysfunction. Chronic obstruction Medicina 2021, 57, 355 of proximal pulmonary vessels by fibrotic clots, development of small vessel disease,3 ofand 12 progressive diffuse remodeling of the pulmonary vasculature collectively represent the pathophysiology of CTEPH [10,11]. Nonresolution of thrombus after PE occurs only in a minority of patients. This leads to failureNonresolution in the restoration of thrombus of normal after PEhemodynamics occurs only in in a the minority pulmonary of patients. circulatory This leads sys- tem.to failure In acute in the PE, restoration fresh red clots of normal made hemodynamicsof red blood cells in and the pulmonaryfibrin mesh circulatory are easily detach- system. ableIn acute from PE, the fresh wall redof the clots pulmonary made of red vessels. blood In cells contrast, and fibrin chronic mesh clots are are easily yellow-colored detachable andfrom composed the wall of of the abundant pulmonary inflammatory vessels. In cells, contrast, elastin, chronic and collagen clots are fibers yellow-colored [10,12]. Further and organizationcomposed of of abundant the chronic inflammatory clot impairs cells, blood elastin, flow andand collagenleads to fibersCTEPH [10 development.,12]. Further Thisorganization organization of the and chronic fibrosis clot represent impairs the blood characteristic flow and bands leads and to CTEPH webs in development. a pulmonary This organization and fibrosis represent the characteristic bands and
Load more

Recommended publications
  • Pleural Effusion and Ventilation/Perfusion Scan Interpretation for Acute Pulmonary Embolus
    ventricular function by radionuclide angiography during exercise in normal subjects 33. Verani MS. Myocardial perfusion imaging versus two-dimensional echocardiography: and patients with chronic coronary heart disease. J Am Coll Cardiol 1983;1:1518- comparative value in the diagnosis of coronary artery disease. J NucíCardiol 1529. 1994;1:399-414. 29. Adam WE. Tarkowska A, Bitter F, Stauch M, Geffers H. Equilibrium (gated) 34. Foster T, McNeill AJ, Salustri A, et al. Simultaneous dobutamine stress echocardiog radionuclide ventriculography. Cardiovasc Radial 1979;2:161-173. raphy and technetium-99m SPECT in patients with suspected coronary artery disease. 30. Hurwitz RA, TrêvesS, Kuroc A. Right ventricular and left ventricular ejection fraction J Am Coll Cardiol I993;21:1591-I596. in pediatrie patients with normal hearts: first pass radionuclide angiography. Am 35. Marwick TH, D'Hondt AM, Mairesse GH, Baudhuin T, Wijins W, Detry JM, Meiin Heart J 1984;107:726-732. 31. Freeman ML, Palac R, Mason J, et al. A comparison of dobutamine infusion and JA. Comparative ability of dobutamine and exercise stress in inducing myocardial ischemia in active patients. Br Heart J 1994:72:31-38. supine bicycle exercise for radionuclide cardiac stress testing. Clin NucíMed 1984:9:251-255. 36. Senior R, Sridhara BS, Anagnostou E, Handler C, Raftery EB, Lahiri A. Synergistic 32. Cohen JL, Greene TO, Ottenweller J, Binebaum SZ, Wilchfort SD, Kim CS. value of simultaneous stress dobutamine sestamibi single-photon-emission computer Dobutamine digital echocardiography for detecting coronary artery disease. Am J ized tomography and echocardiography in the detection of coronary artery disease.
    [Show full text]
  • Diagnosing Pulmonary Embolism M Riedel
    309 Postgrad Med J: first published as 10.1136/pgmj.2003.007955 on 10 June 2004. Downloaded from REVIEW Diagnosing pulmonary embolism M Riedel ............................................................................................................................... Postgrad Med J 2004;80:309–319. doi: 10.1136/pgmj.2003.007955 Objective testing for pulmonary embolism is necessary, embolism have a low long term risk of subse- quent VTE.2 5–7 because clinical assessment alone is unreliable and the consequences of misdiagnosis are serious. No single test RISK FACTORS AND RISK has ideal properties (100% sensitivity and specificity, no STRATIFICATION risk, low cost). Pulmonary angiography is regarded as the The factors predisposing to VTE broadly fit Virchow’s triad of venous stasis, injury to the final arbiter but is ill suited for diagnosing a disease vein wall, and enhanced coagulability of the present in only a third of patients in whom it is suspected. blood (box 1). The identification of risk factors Some tests are good for confirmation and some for aids clinical diagnosis of VTE and guides decisions about repeat testing in borderline exclusion of embolism; others are able to do both but are cases. Primary ‘‘thrombophilic’’ abnormalities often non-diagnostic. For optimal efficiency, choice of the need to interact with acquired risk factors before initial test should be guided by clinical assessment of the thrombosis occurs; they are usually discovered after the thromboembolic event. Therefore, the likelihood of embolism and by patient characteristics that risk of VTE is best assessed by recognising the may influence test accuracy. Standardised clinical presence of known ‘‘clinical’’ risk factors. estimates can be used to give a pre-test probability to However, investigations for thrombophilic dis- orders at follow up should be considered in those assess, after appropriate objective testing, the post-test without another apparent explanation.
    [Show full text]
  • An Interesting Case of Undiagnosed Pleural Effusion Case Report
    Amit Panjwani, Thuraya Zaid [email protected] Pulmonary Medicine, Salmaniya Medical Complex, Manama, Bahrain. An interesting case of undiagnosed pleural effusion Case report Pleural effusions are commonly encountered in the Investigations revealed a haemoglobin level Cite as: Panjwani A, Zaid T. clinical practise of both respiratory and nonrespiratory of 16.4 g⋅dL−1, and total leukocyte count of An interesting case of specialists. An estimated 1–1.5 million new cases in 8870 cells⋅mm−3 with a differential count of 62% undiagnosed pleural effusion. the USA and 200 000–250 000 new cases of pleural neutrophils, 28% lymphocytes, 7% monocytes, 2% Breathe 2017; 13: e46–e52. effusions are reported from the UK each year [1]. eosinophils and 1% basophils. The platelet count Analysis of the relevant clinical history, physical was 160 000 cells⋅mm−3. Creatinine, electrolytes examination, chest radiography and diagnostic and liver function tests were normal. The ECG was thoracentesis is useful in identifying the cause of unremarkable and cardiac enzymes were within pleural effusion in majority of the cases [2]. In a few normal limits. Chest radiograph (figure 1) showed a cases, the aetiology may be unclear after the initial mild, right-sided pleural effusion, blunting of the left assessment. The list of diseases that may account for costophrenic angle, no shift of mediastinal position a persistent undiagnosed pleural effusion is long [3]. and no lung parenchymal opacities. We present an interesting case of undiagnosed pleural effusion that was encountered in our hospital. R Case presentation A 33-year-old male presented to our hospital with a history of sudden-onset, pleuritic, right-sided chest pain of 2 days’ duration.
    [Show full text]
  • Diagnosis of Chronic Thromboembolic Pulmonary Hypertension After Acute Pulmonary Embolism
    Early View Review Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism Fredrikus A. Klok, Francis Couturaud, Marion Delcroix, Marc Humbert Please cite this article as: Klok FA, Couturaud F, Delcroix M, et al. Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism. Eur Respir J 2020; in press (https://doi.org/10.1183/13993003.00189-2020). This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Copyright ©ERS 2020 Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism Fredrikus A. Klok, Francis Couturaud F2, Marion Delcroix M3, Marc Humbert4-6 1 Department of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, The Netherlands 2 Département de Médecine Interne et Pneumologie, Centre Hospitalo-Universitaire de Brest, Univ Brest, EA 3878, CIC INSERM1412, Brest, France 3 Department of Respiratory Diseases, University Hospitals and Respiratory Division, Department of Chronic Diseases, Metabolism & Aging, KU Leuven – University of Leuven, Leuven, Belgium 4 Université Paris-Saclay, Faculté de Médecine, Le Kremlin-Bicêtre, France 5 Service de Pneumologie et Soins Intensifs Respiratoires, Hôpital Bicêtre, AP-HP, Le Kremlin-Bicêtre, France 6 INSERM UMR S 999, Hôpital Marie Lannelongue, Le Plessis Robinson, France Corresponding author: Frederikus A. Klok, MD, FESC; Department of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands; Albinusdreef 2, 2300RC, Leiden, the Netherlands; Phone: +31- 715269111; E-mail: [email protected] Abstract Chronic thromboembolic pulmonary hypertension (CTEPH) is the most severe long-term complication of acute pulmonary embolism (PE).
    [Show full text]
  • Acute Pulmonary Embolism in Patients with and Without COVID-19
    Journal of Clinical Medicine Article Acute Pulmonary Embolism in Patients with and without COVID-19 Antonin Trimaille 1,2 , Anaïs Curtiaud 1, Kensuke Matsushita 1,2 , Benjamin Marchandot 1 , Jean-Jacques Von Hunolstein 1 , Chisato Sato 1,2, Ian Leonard-Lorant 3, Laurent Sattler 4 , Lelia Grunebaum 4, Mickaël Ohana 3 , Patrick Ohlmann 1 , Laurence Jesel 1,2 and Olivier Morel 1,2,* 1 Division of Cardiovascular Medicine, Nouvel Hôpital Civil, Strasbourg University Hospital, 67000 Strasbourg, France; [email protected] (A.T.); [email protected] (A.C.); [email protected] (K.M.); [email protected] (B.M.); [email protected] (J.-J.V.H.); [email protected] (C.S.); [email protected] (P.O.); [email protected] (L.J.) 2 INSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, 67000 Strasbourg, France 3 Radiology Department, Nouvel Hôpital Civil, Strasbourg University Hospital, 67000 Strasbourg, France; [email protected] (I.L.-L.); [email protected] (M.O.) 4 Haematology and Haemostasis Laboratory, Centre for Thrombosis and Haemostasis, Nouvel Hôpital Civil, Strasbourg University Hospital, 67000 Strasbourg, France; [email protected] (L.S.); [email protected] (L.G.) * Correspondence: [email protected] Abstract: Introduction. Acute pulmonary embolism (APE) is a frequent condition in patients with Citation: Trimaille, A.; Curtiaud, A.; COVID-19 and is associated with worse outcomes. Previous studies suggested an immunothrombosis Matsushita, K.; Marchandot, B.; instead of a thrombus embolism, but the precise mechanisms remain unknown.
    [Show full text]
  • Right Heart Pressures in Bronchial Asthma
    Thorax: first published as 10.1136/thx.26.1.39 on 1 January 1971. Downloaded from Thorax (1971), 26, 39. Right heart pressures in bronchial asthma R. F. GUNSTONE St. George's Hospital, London S.W.1 Right heart pressures, electrocardiograms, blood gases, and peak expiratory flow rates were measured in nine patients admitted to hospital with severe bronchial asthma. Low or normal right heart pressures were found despite electrocardiographic changes in five patients consisting of right atrial P waves, abnormal right axis deviation, and in one patient T-wave changes in pre- cordial leads. These electrocardiographic changes reverted towards normal on recovery of the patient from the asthmatic attack. Electrocardiographic changes suggestive of right The procedure was carried out in the general ward heart embarrassment have been noted in acute with the patient in the sitting position supported at 60 bronchial asthma, particularly right atrial P waves to 90 degrees to the horizontal because orthopnoea (P and abnormal right axis deviation was always present. Immediately after catheterization pulmonale) the peak expiratory flow rate was measured with a (Harkavy and Romanoff, 1942; Miyamato, Wright peak flow meter (Wright and McKerrow, Bastaroli, and Hoffman, 1961; Ambiavagar, 1959) and blood (capillary or arterial) was taken for Jones and Roberts, 1967). These observations measurement of pH, Pco2, and standard bicarbonate raise the possibility that death in bronchial asthma by the Astrup method (Astrup, J0rgensen, Andersen, may be due to acute cor pulmonale although and Engel, 1960). The peak flow rate and electro- copyright. necropsy evidence is against this suggestion (Earle, cardiogram were repeated after recovery.
    [Show full text]
  • Severe Asthma Is Associated with a Remodeling of the Pulmonary Arteries in Horses
    bioRxiv preprint doi: https://doi.org/10.1101/2020.04.15.042903; this version posted April 17, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Severe asthma is associated with a remodeling of the pulmonary arteries in horses Remodeling of pulmonary arteries in severe equine asthma Serena Ceriotti1,2, Michela Bullone1, Mathilde Leclere1, Francesco Ferrucci2, Jean-Pierre Lavoie1* 1 Department of Clinical Sciences, Faculty of Veterinary Medicine, University of Montreal, Saint- Hyacinthe, Quebec, Canada 2 Department of Health, Animal Science and Food Safety, Università degli Studi di Milano, Milano, Italy Dr. Ceriotti current address is Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, Alabama, USA Dr. Bullone current address is Department of Veterinary Science, Università degli Studi di Torino, Grugliasco, Italy *Corresponding author: [email protected] Serena Ceriotti and Jean-Pierre Lavoie conceived and designed the work. Serena Ceriotti, Michela Bullone and Mathilde Leclere acquired clinical data, collected, processed and prepared histological and immunostained samples. Serena Ceriotti performed histomorphometric studies and statistical analysis. Serena Ceriotti, Jean-Pierre Lavoie and Francesco Ferrucci prepared and edited the manuscript prior to submission. Michela Bullone and Mathilde Leclere edited the manuscript prior to submission. 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.04.15.042903; this version posted April 17, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.
    [Show full text]
  • COVID-19 Associated Pulmonary Embolism in Pediatric Patients
    Prepublication Release A N O F F I C I A L J O U R N A L O F T H E A M E R I C A N A C A D E M Y O F P E D I A T R I C S COVID-19 Associated Pulmonary Embolism in Pediatric Patients Melissa Chima, Duane Williams, Neal J. Thomas, Conrad Krawiec DOI: 10.1542/hpeds.2021-005866 Journal: Hospital Pediatrics Article Type: Original Article Citation: Chima M, et al. COVID-19 Associated Pulmonary Embolism in Pediatric Patients. Hosp Pediatr. 2021; doi: 10.1542/hpeds.2021-005866 This is a prepublication version of an article that has undergone peer review and been accepted for publication but is not the final version of record. This paper may be cited using the DOI and date of access. This paper may contain information that has errors in facts, figures, and statements, and will be corrected in the final published version. The journal is providing an early version of this article to expedite access to this information. The American Academy of Pediatrics, the editors, and authors are not responsible for inaccurate information and data described in this version. Downloaded©202 from1 www.aappublications.org/news American Academy byof guest Pediatrics on October 1, 2021 Prepublication Release COVID-19 Associated Pulmonary Embolism in Pediatric Patients Melissa Chima, BS1, Duane Williams, MD2, Neal J. Thomas, MD2,3, Conrad Krawiec, MD2 Authors’ Affiliations and Addresses: 1Penn State College of Medicine, 500 University Drive, P.O. Box 850, Hershey, PA, USA 17033-0850, Tel: (717)-531-5337, Fax: (717)-531-8985.
    [Show full text]
  • Pulmonary Embolism Or Pneumocystis Jiroveci Pneumonia?
    breathe case presentations.qxd 26/07/2006 12:03 Page 5 CASE PRESENTATION Pulmonary embolism or Pneumocystis jiroveci pneumonia? Case report Table 1 Vital signs and F. Braiteh1,2 A 33-year-old male presented to the emergency laboratory test results at I. Nash3 department with a 5-day history of exertional dys- presentation pnoea, dry cough, lethargy and an ongoing fever of 38.9°C. He had been previously diagnosed Investigation Result Normal 1Medical Oncology, Division of with left-frontal oligodendroglioma during a range Cancer Medicine, The University work-up following a new-onset seizure 4 months Vital signs of Texas M.D. Anderson Cancer Temperature °C 36.6 earlier. After successful tumour resection and Center, 2University of Texas Respiratory rate cycles·min-1 22 adjuvant radiotherapy, the patient totally recov- Graduate School of Biomedical Heart rate beats·min-1 88 ered without any residual paresis. He was main- Sciences, Houston, TX, and Blood pressure mmHg 126/64 3Dept of Pathology, Hospital of tained on valproic acid and dexamethasone at a O2 saturation % 91 Saint Raphael, Yale School of -1 dose that was tapered down to 2 mg·day . Haematological counts and coagulation Medicine, New Haven, CT, USA. The physical examination was unremarkable. White cells ×109·L -1 6.8 4.0–10.0 The patient was haemodynamically stable but Platelets ×109·L -1 123 150–350 hypoxaemic and anaemic (table 1). Chest radio- Haemoglobin g·dL-1 9.3 12.0–16.0 Correspondence: graphy and computed tomography (CT) were Prothrombine time s 12.8 <13.0 F.
    [Show full text]
  • Pulmonary Embolism (Pe): Diagnosis
    PULMONARY EMBOLISM (PE): DIAGNOSIS OBJECTIVE: To provide a diagnostic approach to patients with suspected acute pulmonary embolism (PE). BACKGROUND: Venous thromboembolism (VTE), which comprises deep vein thrombosis (DVT) and pulmonary embolism (PE), is a common disease, affecting approximately 1-2 in 1,000 adults per year. The diagnosis of PE has increased significantly since the advent of computed tomography pulmonary angiography (CTPA) with its widespread availability and enhanced sensitivity. The majority of PE originates in the proximal deep veins of the leg, despite the observation that only 25-50% of patients with PE have clinically evident DVT at the time of PE diagnosis. While active malignancy, surgery (especially orthopedic), hospitalization, air travel >8 hours, and hormone use/pregnancy are common transient provoking factors, approximately 50% of first-time PEs appear to be unprovoked. Symptoms of PE may include sudden onset dyspnea, pleuritic chest pain, and syncope. Signs of PE may include tachypnea, tachycardia, hypoxemia, hypotension, and features of right ventricular dysfunction (distended jugular veins). There may be accompanying signs and symptoms of DVT. The ECG may show right ventricular strain (S1Q3T3, right bundle branch block and T-inversion in leads V1- V4). Up to 10% of symptomatic PEs are fatal within the first hour of symptom onset. Independent predictors of mortality within the first few days after diagnosis of PE include hypotension (systolic blood pressure [SBP] <90 mmHg), clinical right heart failure, right ventricular dilatation on CTPA/echocardiography, positive troponin, and elevated brain natriuretic peptide (BNP). Early diagnosis and treatment of PE reduces morbidity and mortality. DIAGNOSIS OF PE: The constellation of symptoms and signs may be suggestive of PE but do not alone have the sensitivity or specificity to rule in or rule out the diagnosis.
    [Show full text]
  • Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE)
    How can it be prevented? You can take steps to prevent deep vein thrombosis (DVT) and pulmonary embolism (PE). If you're at risk for these conditions: • See your doctor for regular checkups. • Take all medicines as your doctor prescribes. • Get out of bed and move around as soon as possible after surgery or illness (as your doctor recommends). Moving around lowers your chance of developing a blood clot. References: • Exercise your lower leg muscles during Deep Vein Thrombosis: MedlinePlus. (n.d.). long trips. Walking helps prevent blood Retrieved October 18, 2016, from clots from forming. https://medlineplus.gov/deepveinthrombos is.html If you've had DVT or PE before, you can help prevent future blood clots. Follow the steps What Are the Signs and Symptoms of Deep above and: Vein Thrombosis? - NHLBI, NIH. (n.d.). Retrieved October 18, 2016, from • Take all medicines that your doctor http://www.nhlbi.nih.gov/health/health- prescribes to prevent or treat blood clots topics/topics/dvt/signs • Follow up with your doctor for tests and treatment Who Is at Risk for Deep Vein Thrombosis? - • Use compression stockings as your DEEP NHLBI, NIH. (n.d.). Retrieved October 18, doctor directs to prevent leg swelling 2016, from http://www.nhlbi.nih.gov/health/health- VEIN topics/topics/dvt/atrisk THROMBOSIS How Can Deep Vein Thrombosis Be Prevented? - NHLBI, NIH. (n.d.). Retrieved October 18, 2016, from (DVT) http://www.nhlbi.nih.gov/health/health- topics/topics/dvt/prevention How Is Deep Vein Thrombosis Treated? - NHLBI, NIH. (n.d.). Retrieved October 18, 2016, from http://www.nhlbi.nih.gov/health/health- topics/topics/dvt/treatment Trinity Surgery Center What is deep vein Who is at risk? What are the thrombosis (DVT)? The risk factors for deep vein thrombosis symptoms? (DVT) include: Only about half of the people who have DVT A blood clot that forms in a vein deep in the • A history of DVT.
    [Show full text]
  • Allergic Bronchopulmonary Aspergillosis: Diagnostic and Treatment Challenges
    y & Re ar sp Leonardi et al., J Pulm Respir Med 2016, 6:4 on ir m a l to u r P y DOI: 10.4172/2161-105X.1000361 f M o e Journal of l d a i n c r i n u e o J ISSN: 2161-105X Pulmonary & Respiratory Medicine Review Article Open Access Allergic Bronchopulmonary Aspergillosis: Diagnostic and Treatment Challenges Lucia Leonardi*, Bianca Laura Cinicola, Rossella Laitano and Marzia Duse Department of Pediatrics and Child Neuropsychiatry, Division of Allergy and Clinical Immunology, Sapienza University of Rome, Policlinico Umberto I, Rome, Italy Abstract Allergic bronchopulmonary aspergillosis (ABPA) is a pulmonary disorder, occurring mostly in asthmatic and cystic fibrosis patients, caused by an abnormal T-helper 2 lymphocyte response of the host to Aspergillus fumigatus antigens. ABPA diagnosis is defined by clinical, laboratory and radiological criteria including active asthma, immediate skin reactivity to A. fumigatus antigens, total serum IgE levels>1000 IU/mL, fleeting pulmonary parenchymal opacities and central bronchiectases that represent an irreversible complication of ABPA. Despite advances in our understanding of the role of the allergic response in the pathophysiology of ABPA, pathogenesis of the disease is still not completely clear. In addition, the absence of consensus regarding its prevalence, diagnostic criteria and staging limits the possibility of diagnosing the disease at early stages. This may delay the administration of a therapy that can potentially prevent permanent lung damage. Long-term management is still poorly studied. Present primary therapies, based on clinical experience, are not yet standardized. These consist in oral corticosteroids, which control acute symptoms by mitigating the allergic inflammatory response, azoles and, more recently, anti-IgE antibodies.
    [Show full text]