acute myocardial infarction. Cardiogenic shock is the largest cause of in-hospitalmortality.[30][73] Rupture of the ventricular dividing wall or left ventricular wall may occurwithin the initial weeks.[73] Dressler's syndrome, a reaction following larger infarcts and a causeof pericarditis is also possible.[73]Heart failure may develop as a long-term consequence, with an impaired ability of heart muscleto pump, scarring, and an increase in the size of the existing muscle. Aneurysm of the leftventricle myocardium develops in about 10% of MI and is itself a risk factor for heart failure,ventricular arrhythmia, and the development of clots.[16]Risk factors for complications and death include age, hemodynamic parameters (such as heartfailure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease, and elevation ofcardiac markers.[141][142][143]Myocardial infarction is a common presentation of coronary artery disease. The World HealthOrganization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heartdisease;[144] with it being the leading cause of death in high- or middle-income countries andsecond only to lower respiratory infections in lower-income countries.[144] Worldwide, morethan 3 million people have STEMIs and 4 million have NSTEMIs a year.[18] STEMIs occur abouttwice as often in men as women.[19]Rates of death from ischemic heart disease (IHD) have slowed or declined in most high-incomecountries, although cardiovascular disease still accounted for one in three of all deaths in the USin 2008.[145] For example, rates of death from cardiovascular disease have decreased almost athird between 2001 and 2011 in the United States.[146]In contrast, IHD is becoming a more common cause of death in the developing world. Forexample, in India, IHD had become the leading cause of death by 2004, accounting for 1.46million deaths (14% of total deaths) and deaths due to IHD were expected to double during1985–2015.[147] Globally, disability adjusted life years (DALYs) lost to ischemic heart disease arepredicted to account for 5.5% of total DALYs in 2030, making it the second-most-importantcause of disability (after unipolar depressive disorder), as well as the leading cause of death bythis date.[144]Social determinants such as neighborhood disadvantage, immigration status, lack of socialsupport, social isolation, access to health services play an important role in myocardial infarctionrisk and survival.[148][149][150][151] Studies have shown that low socioeconomic status isassociated with an increased risk of poorer survival. There are well-documented disparities inmyocardial infarction survival by socioeconomic status, race, education, and census-tract-levelpoverty.[152]Race: In the U.S. African Americans have a greater burden of myocardial infarction and othercardiovascular events. On a population level, there is a higher overall prevalence of risk factorsthat are unrecognized and therefore not treated, which places these individuals at a greaterlikelihood of experiencing adverse outcomes and therefore potentially higher morbidity andmortality.[153]EpidemiologySocial determinants of health
Socioeconomic status: Among individuals who live in the low-socioeconomic (SES) areas, whichis close to 25% of the US population, myocardial infarctions (MIs) occurred twice as oftencompared with people who lived in higher SES areas.[154]Immigration status: In 2018 many lawfully present immigrants who are eligible for coverageremain uninsured because immigrant families face a range of enrollment barriers, including fear,confusion about eligibility policies, difficulty navigating the enrollment process, and languageand literacy challenges. Uninsured undocumented immigrants are ineligible for coverage optionsdue to their immigration status.[155]Health care access: Lack of health insurance and financial concerns about accessing care wereassociated with delays in seeking emergency care for acute myocardial infarction which can havesignificant, adverse consequences on patient outcomes.[156]Education: Researchers found that compared to people with graduate degrees, those with lowereducational attainment appeared to have a higher risk of heart attack, dying from acardiovascular event, and overall death.[157]Depictions of heart attacks in popular media often include collapsing or loss of consciousnesswhich are not common symptoms; these depictions contribute to widespread misunderstandingabout the symptoms of myocardial infarctions, which in turn contributes to people not gettingcare when they should.[158]At common law, in general, a myocardial infarction is a disease, but may sometimes be an injury.This can create coverage issues in the administration of no-fault insurance schemes such asworkers' compensation. In general, a heart attack is not covered;[159] however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion.[160]In addition, in some jurisdictions, heart attacks suffered by persons in particular occupationssuch as police officers may be classified as line-of-duty injuries by statute or policy. In somecountries or states, a person having suffered from an MI may be prevented from participating inactivity that puts other people's lives at risk, for example driving a car or flying an airplane.[161]1. \"What Are the Signs and Symptoms of Coronary Heart Disease?\" (https://web.archive.org/web/20150224034615/http://www.nhlbi.nih.gov/health/health-topics/topics/cad/signs).www.nhlbi.nih.gov. September 29, 2014. Archived from the original (http://www.nhlbi.nih.gov/health/health-topics/topics/cad/signs) on 24 February 2015. Retrieved 23 February 2015.2. \"Heart Attack Symptoms in Women\" (https://www.heart.org/en/health-topics/heart-attack/warning-signs-of-a-heart-attack/heart-attack-symptoms-in-women). American Heart Association.3. \"What Is a Heart Attack?\" (http://www.nhlbi.nih.gov/health/health-topics/topics/heartattack/).www.nhlbi.nih.gov. December 17, 2013. Archived (https://web.archive.org/web/20150219152830/http://www.nhlbi.nih.gov/health/health-topics/topics/heartattack/) from the original on 19February 2015. Retrieved 24 February 2015.Society and cultureLegal implicationsReferences
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Classification ICD-10: I21 (https://icd.who.int/browse10/2019/en#/I21)-I22 (https://icd.who.int/browse10/2019/en#/I22) · ICD-9-CM:410 (http://www.icd9data.com/getICD9Code.ashx?icd9=410) · MeSH:D009203 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&term=D009203) ·DiseasesDB: 8664(http://www.diseasesdatabase.com/ddb8664.htm)ExternalresourcesMedlinePlus:000195 (https://www.nlm.nih.gov/medlineplus/ency/article/000195.htm) ·Braunwald's Heart Disease (https://books.google.com/books?id=0TzrjwEACAAJ). Elsevier.pp. 295–313. ISBN 978-0-323-35943-6.Morrow DA, Braunwald E (15 September 2016). \"Classification and Diagnosis of AcuteCoronary Syndromes\". In Morrow DA (ed.). Myocardial Infarction: A Companion toBraunwald's Heart Disease (https://books.google.com/books?id=0TzrjwEACAAJ). Elsevier.pp. 1–10. ISBN 978-0-323-35943-6.Morrow DA (15 September 2016). \"Clinical Approach to Suspected Acute MyocardialInfarction\". In Morrow DA (ed.). Myocardial Infarction: A Companion to Braunwald's HeartDisease (https://books.google.com/books?id=0TzrjwEACAAJ). Elsevier. pp. 55–65.ISBN 978-0-323-35943-6.Levine GN, Bates ER, Blankenship JC, Bailey SR, Bittl JA, Cercek B, et al. (March 2016).\"2015 ACC/AHA/SCAI Focused Update on Primary Percutaneous Coronary Intervention forPatients With ST-Elevation Myocardial Infarction: An Update of the 2011 ACCF/AHA/SCAIGuideline for Percutaneous Coronary Intervention and the 2013 ACCF/AHA Guideline for theManagement of ST-Elevation Myocardial Infarction: A Report of the American College ofCardiology/American Heart Association Task Force on Clinical Practice Guidelines and theSociety for Cardiovascular Angiography and Interventions\" (https://doi.org/10.1161%2FCIR.0000000000000336). Circulation. 133 (11): 1135–47. doi 10.1161/CIR.0000000000000336 (htt:ps://doi.org/10.1161%2FCIR.0000000000000336) PMID 26490017 (https://pubmed.ncbi.nl. m.nih.gov/26490017).Myocardial infarction (https://curlie.org/Health/Conditions_and_Diseases/Cardiovascular_Disorders/Heart_Disease) atCurlieAmerican Heart Association's Heart Attack web site (http://www.americanheart.org/heartattack) — Information andresources for preventing, recognizing, and treating a heartattack.TIMI Score for UA/NSTEMI (http://www.mdcalc.com/timi-risk-score-for-uanstemi/) and STEMI (http://www.mdcalc.com/timi-risk-score-for-stemi/)HEART Score for Major Cardiac Events (http://www.mdcalc.com/heart-score-for-major-cardiac-events/)\"Heart Attack\" (https://medlineplus.gov/heartattack.html).MedlinePlus. U.S. National Library of Medicine.Further readingExternal linksD
eMedicine:med/1567 (https://emedicine.medscape.com/med/1567-overview) emerg/327(http://www.emedicine.com/emerg/topic327.htm#)ped/2520 (http://www.emedicine.com/ped/topic2520.htm#)· Patient UK:Myocardialinfarction (https://patient.info/doctor/acute-myocardial-infarction)Retrieved from \"https://en.wikipedia.org/w/index.php?title=Myocardial_infarction&oldid=1043418446\"This page was last edited on 10 September 2021, at 01:19 (UTC).Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By usingthis site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the WikimediaFoundation, Inc., a non-profit organization.
PetechiaOther namesPetechiaePetechia and purpura on the low limb due tomedication-induced vasculitisPronunciationpetechia /pɪˈtiːkiə/ petechiae/pɪˈtiːkiiː/SpecialtyRheumatologyPetechiaA petechia (pl. petechiae) is a small (1–2 mm)red or purple spot on the skin or conjunctiva,caused by a minor bleed from broken capillaryblood vessels. The word is derived from Latin[1]'petigo', meaning ‘scab' or 'eruption’.Petechia refers to one of the three descriptivetypes of hematoma differentiated by size, the othertwo being ecchymosis and purpura. Ecchymosis isdefined as hematomas larger than 1 centimetre[1]and purpura as 1–5 millimetres.[2]The term is almost always used in the plural(petechiae), since a single lesion is seldom noticedor significant.CausesPhysical traumaNon-infectious conditionsInfectious conditionsForensic scienceSee alsoReferencesExternal linksThe most common cause of petechiae is through physical trauma such as a hard bout ofcoughing, holding breath, vomiting, or crying, which can result in facial petechiae, especiallyaround the eyes. Such instances are harmless and usually disappear within a few days.Constriction, Asphyxiation – Petechiae, especially in the eyes, may also occur whenexcessive pressure is applied to tissue (e.g., when a tourniquet is applied to an extremity orwith excessive coughing or vomiting).Sunburn, childbirth, weightlifting[3]Gua Sha, a Chinese treatment that scrapes the skinHigh-G trainingHickeyContentsCausesPhysical trauma
AsphyxiationChoking gameOral sex[4]Vitamin C deficiency, scurvy[3]Vitamin K deficiency[3]Leukemia[3]Thrombocytopenia – Low platelet counts or diminished platelet function (e.g., as a side effectof medications or during certain infections) can give rise to petechial spots[1]clotting factor deficiencies – (Von Willebrand disease)HypocalcemiaIdiopathic thrombocytopenic purpuraCoeliac diseaseAplastic anaemiaLupusKwashiorkor or Marasmus – Childhood protein-energy malnutritionErythroblastosis fetalisHenoch–Schönlein purpuraKawasaki diseaseSchamberg diseaseEhlers–Danlos syndromeSjögren syndrome – Petechial spots could occur due to vasculitis, an inflammation of theblood vessels. In such a case immediate treatment is needed to prevent permanent damage.Some malignancies can also cause petechiae to appear.RadiationHavana syndromeBabesiosisBolivian hemorrhagic feverBoutonneuse feverChikungunyaCerebral malariaCongenital syphilisCrimean–Congo hemorrhagic feverCytomegalovirusDengue feverDukes' diseaseEbolaEndocarditisInfluenza A virus subtype H1N1HantavirusInfectious mononucleosisNon-infectious conditionsInfectious conditions
Palatal petechiae.Marburg virusNeisseria meningitidisRocky Mountain spotted feverScarlet feverTyphus[5]Streptococcal pharyngitis – Petechiae on the soft palateare mainly associated with streptococcal pharyngitis,[6]and as such it is an uncommon but highly specificfinding.[7]Petechiae on the face and conjunctiva (eyes) are unrelated toasphyxiation or hypoxia.[8]Despite this, petechiae are used by police investigators indetermining whether strangulation has been part of anattack. The documentation of the presence of petechiae on avictim can help police investigators prove the case.[9] Petechiae resulting from strangulation canbe relatively tiny and light in color to very bright and pronounced. Petechiae may be seen on theface, in the whites of the eyes or on the inside of the eyelids.Purpura, which is the mid-sized type of hematoma (3–10 mm)Ecchymoses, which is the large type of hematoma (>1 cm)1. Kumar, Vinay (2017). Robbins Basic Pathology. Abbas, Abul K.; Aster, Jon C.; Perkins,James A. (10th ed.). Philadelphia, PA. p. 101. ISBN 978-0323353175 OCLC 960844656 (htt. ps://www.worldcat.org/oclc/960844656).2. McKenzie, Shirlyn B. (2014). Clinical Laboratory Hematology. Williams, Joanne Lynne;Landis-Piwowar, Kristin (3rd ed.). Boston, MA. p. 665. ISBN 978-0133076011.OCLC 878098857 (https://www.worldcat.org/oclc/878098857).3. \"Causes\" (http://www.mayoclinic.org/symptoms/petechiae/basics/causes/sym-20050724).4. Schlesinger, SL; Borbotsina, J; O'Neill, L (September 1975). \"Petechial hemorrhages of thesoft palate secondary to fellatio\". Oral Surgery, Oral Medicine, and Oral Pathology. 40 (3):376–78. doi 10.1016/0030-4220(75)90422-3 (https://doi.org/10.1016%2F0030-4220%2875%:2990422-3) PMID 1080847 (https://pubmed.ncbi.nlm.nih.gov/1080847). .5. Grayson MD, Charlotte (2006-09-26). \"Typhus\" (https://www.nlm.nih.gov/medlineplus/ency/article/001363.htm). MedlinePlus Medical Encyclopedia. National Institutes of Health.Retrieved 2007-11-05.6. Fact Sheet: Tonsillitis (http://www.entnet.org/HealthInformation/tonsillitis.cfm) from AmericanAcademy of Otolaryngology. \"Updated 1/11\". Retrieved November 20117. Brook I, Dohar JE (December 2006). \"Management of group A beta-hemolytic streptococcalpharyngotonsillitis in children\". J Fam Pract. 55 (12): S1–11, quiz S12. PMID 17137534 (https://pubmed.ncbi.nlm.nih.gov/17137534).8. Ely, Susan F.; Charles S. Hirsch (2000). \"Asphyxial deaths and petechiae: a review\" (http://www.charlydmiller.com/LIB04/2000petechiaereview.pdf) (PDF). Journal of Forensic Sciences.Forensic scienceSee alsoReferences
Classification ICD-10: R23.3 (https://icd.who.int/browse10/2019/en#/R23.3) · ICD-9-CM:782.7 (http://www.icd9data.com/getICD9Code.ashx?icd9=782.7) · MeSH:D011693 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&term=D011693)45 (6): 1274–1277. doi 10.1520/JFS14878J (https://doi.org/10.1520%2FJFS14878J):.Retrieved 2007-09-22.9. \"Investigating Domestic Violence Strangulation\" (http://www.bluesheepdog.com/2007/11/09/investigating-domestic-violence-strangulation-what-is-it-and-how-to-recognize-it/).BlueSheepdog.com. 2007-11-09. Retrieved 12 May 2011.Retrieved from \"https://en.wikipedia.org/w/index.php?title=Petechia&oldid=1043655153\"This page was last edited on 11 September 2021, at 07:29 (UTC).Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By usingthis site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the WikimediaFoundation, Inc., a non-profit organization.External linksD
Pulmonary embolismA lung illustration depicting a pulmonary embolismas a thrombus (blood clot) that has travelled fromanother region of the body, causes occlusion of thepulmonary bronchial artery, leading to arterialthrombosis of the superior and inferior lobes in theleft lungSpecialtyHematology, cardiology,pulmonologySymptomsShortness of breath, chest pain,coughing up blood[1]ComplicationsPassing out, abnormally low bloodpressure, sudden death[2]Usual onsetAdvanced age[3]Risk factorsCancer, prolonged bed rest,smoking, stroke, certain geneticconditions, estrogen-basedmedication, pregnancy, obesity,after surgery[3]DiagnosticmethodBased on symptoms, D-dimer, CTpulmonary angiography, lungventilation/perfusion scan[4]TreatmentAnticoagulants (heparin, warfarin,DOACs)[5]Frequency~450,000 per year (USA), 430,000(Europe)[6][7][8]Deaths>10–12,000 per year (US), >30–[9]40,000 per year (Europe)[10]Pulmonary embolismPulmonary embolism PE () is a blockage ofan artery in the lungs by a substance that hasmoved from elsewhere in the body through thebloodstream (embolism).[6] Symptoms of a PEmay include shortness of breath, chest painparticularly upon breathing in, and coughingup blood. Symptoms of a blood clot in the leg[1]may also be present, such as a red, warm,swollen, and painful leg. Signs of a PE[1]include low blood oxygen levels, rapidbreathing, rapid heart rate, and sometimes amild fever.[11] Severe cases can lead to passingout, abnormally low blood pressure, andsudden death.[2]PE usually results from a blood clot in the legthat travels to the lung.[6] The risk of bloodclots is increased by cancer, prolonged bedrest, smoking, stroke, certain geneticconditions, estrogen-based medication,pregnancy, obesity, and after some types ofsurgery.[3] A small proportion of cases are dueto the embolization of air, fat, or amnioticfluid.[12][13] Diagnosis is based on signs andsymptoms in combination with test results.[4]If the risk is low, a blood test known as a D-dimer may rule out the condition.[4]Otherwise, a CT pulmonary angiography, lungventilation/perfusion scan, or ultrasound ofthe legs may confirm the diagnosis.[4]Together, deep vein thrombosis and PE areknown as venous thromboembolism (VTE).[14]Efforts to prevent PE include beginning tomove as soon as possible after surgery, lowerleg exercises during periods of sitting, and theuse of blood thinners after some types ofsurgery.[15] Treatment is with anticoagulantssuch as heparin, warfarin or one of the direct-acting oral anticoagulants (DOACs).[5] Theseare recommended for at least three months.[5]Severe cases may require thrombolysis usingmedication such as tissue plasminogenactivator (tPA) given intravenously or througha catheter, and some may require surgery (a
pulmonary thrombectomy).[16] If blood thinners are not appropriate, a temporary vena cavafilter may be used.[16]Pulmonary emboli affect about 430,000 people each year in Europe.[8] In the United States,between 300,000 and 600,000 cases occur each year,[6][7] which contribute to at least 40,000deaths.[9] Rates are similar in males and females.[3] They become more common as people getolder.[3]Signs and symptomsRisk factorsUnderlying causesDiagnosisProbability testingBlood testsImagingElectrocardiogramEchocardiographyPreventionTreatmentAnticoagulationThrombolysisInferior vena cava filterSurgeryEpidemiologyPrognosisPredicting mortalityReferencesExternal linksSymptoms of pulmonary embolism are typically sudden in onset and may include one or many ofthe following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a\"pleuritic\" nature (worsened by breathing), cough and hemoptysis (coughing up blood).[17] Moresevere cases can include signs such as cyanosis (blue discoloration, usually of the lips andfingers), collapse, and circulatory instability because of decreased blood flow through the lungsand into the left side of the heart. About 15% of all cases of sudden death are attributable toPE.[2] While PE may present with syncope, less than 1% of syncope cases are due to PE.[18]On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub maybe audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion issometimes present that is exudative, detectable by decreased percussion note, audible breathsounds, and vocal resonance. Strain on the right ventricle may be detected as a left parasternalContentsSigns and symptoms
A deep vein thrombosis as seen inthe right leg is a risk factor for PEheave, a loud pulmonary component of the second heart sound, and/or raised jugular venouspressure.[2] A low-grade fever may be present, particularly if there is associated pulmonaryhemorrhage or infarction.[19]As smaller pulmonary emboli tend to lodge in more peripheral areas without collateralcirculation, they are more likely to cause lung infarction and small effusions (both of which arepainful), but not hypoxia, dyspnea, or hemodynamic instability such as tachycardia. Larger PEs,which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, fast heartrate and fainting, but are often painless because there is no lung infarction due to collateralcirculation. The classic presentation for PE with pleuritic pain, dyspnea, and tachycardia is likelycaused by a large fragmented embolism causing both large and small PEs. Thus, small PEs areoften missed because they cause pleuritic pain alone without any other findings and large PEsare often missed because they are painless and mimic other conditions often causing ECGchanges and small rises in troponin and brain natriuretic peptide levels.[20]PEs are sometimes described as massive, submissive, and nonmassive depending on the clinicalsigns and symptoms. Although the exact definitions of these are unclear, an accepted definitionof massive PE is one in which there is hemodynamic instability such as sustained low bloodpressure, slowed heart rate, or pulselessness.[21]About 90% of emboli are from proximal leg deep veinthrombosis (DVTs) or pelvic vein thromboses.[22] DVTs areat risk for dislodging and migrating to the lung circulation.The conditions are generally regarded as a continuumtermed venous thromboembolism (VTE).VTE is much more common in immunocompromisedindividuals as well as individuals with comorbiditiesincluding:Those that undergo orthopedic surgery at or below thehip without prophylaxis.[23]This is due to immobility during or after the surgery,as well as venous damage during the surgery.[23]Pancreatic and colon cancer patients (other forms ofcancer also can be factors, but these are the mostcommon)[23]This is due to the release of procoagulants.[23]Risk of VTE is at its greatest during diagnosis andtreatment, but lowers in remission.[23]Patients with high-grade tumors[23]Pregnant individuals[23]As the body puts itself into what is known as a \"hypercoagulable state\" the risk of ahemorrhage during childbirth is decreased and is regulated by increased expression offactors VII, VIII, X, Von Willebrand, and fibrinogen.[23]Those on estrogen medication[23][24][25][26]Risk factors
The development of thrombosis is classically due to a group of causes named Virchow's triad(alterations in blood flow, factors in the vessel wall, and factors affecting the properties of theblood). Often, more than one risk factor is present.Alterations in blood flow: immobilization (after surgery, long-haul flight), injury, pregnancy(also procoagulant), obesity (also procoagulant), cancer (also procoagulant)Factors in the vessel wall: surgery, catheterizations causing direct injury (\"endothelial injury\")Factors affecting the properties of the blood (procoagulant state):Estrogen-containing medication (transgender hormone therapy, menopausal hormonetherapy and hormonal contraceptives)[25][24][26]Genetic thrombophilia (factor V Leiden, prothrombin mutation G20210A, protein Cdeficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia andplasminogen/fibrinolysis disorders)Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, paroxysmalnocturnal hemoglobinuria)Cancer (due to secretion of pro-coagulants)Although most pulmonary embolisms are the result of proximal leg deep vein thrombosis(DVTs), there are still many other risk factors that can also result in a pulmonary embolism.Risk Factors Include:Varicose veins caused by vascular damage[27]Pulmonary hypertension[27]Diabetes[27]Traumatic hip fractures that immobilize the patient[27]Joint fixation (primarily in the legs)[23]After a first PE, the search for secondary causes is usually brief. Only when a second PE occurs,and especially when this happens while still under anticoagulant therapy, a further search forunderlying conditions is undertaken. This will include testing (\"thrombophilia screen\") forFactor V Leiden mutation, antiphospholipid antibodies, protein C and S and antithrombin levels,and later prothrombin mutation, MTHFR mutation, Factor VIII concentration and rarerinherited coagulation abnormalities.[28]To diagnose a pulmonary embolism, a review of clinical criteria to determine the need for testingis recommended.[29] In those who have low risk, age less than 50, heart rate less than 100 beatsper minute, oxygen level more than 94% on room air, and no leg swelling, coughing up of blood,surgery or trauma in the last four weeks, previous blood clots, or estrogen use, further testing isnot typically needed.[30]In situations with more high risk individuals, further testing is needed. A CT pulmonaryangiogram (CTPA) is the preferred method for diagnosis of a pulmonary embolism due to itseasy administration and accuracy.[31] Although a CTPA is preferred, there are also other teststhat can be done. For example, a proximal lower limb compression ultrasound (CUS) can beused.[31] This is a test which is primarily used as a confirmatory test, meaning it confirms aUnderlying causesDiagnosis
A Hampton hump in a person with aright lower lobe pulmonaryembolismprevious analysis showing the presence or suspectedpresence of a pulmonary embolism.[31] According to a cross-sectional study, CUS tests have a sensitivity of 41% andspecificity of 96%.[31]If there are concerns this is followed by testing to determinea likelihood of being able to confirm a diagnosis by imaging,followed by imaging if other tests have shown that there is alikelihood of a PE diagnosis.[29][32][33]The diagnosis of PE is based primarily on validated clinicalcriteria combined with selective testing because the typicalclinical presentation (shortness of breath, chest pain) cannotbe definitively differentiated from other causes of chest painand shortness of breath. The decision to perform medicalimaging is based on clinical reasoning, that is, the medicalhistory, symptoms, and findings on physical examination,followed by an assessment of clinical probability.[2]The most commonly used method to predict clinical probability, the Wells score, is a clinicalprediction rule, whose use is complicated by multiple versions being available. In 1995, PhilipSteven Wells, initially developed a prediction rule (based on a literature search) to predict thelikelihood of PE, based on clinical criteria.[34] The prediction rule was revised in 1998[35] Thisprediction rule was further revised when simplified during a validation by Wells et al. in2000.[36] In the 2000 publication, Wells proposed two different scoring systems using cutoffs of2 or 4 with the same prediction rule.[36] In 2001, Wells published results using the moreconservative cutoff of 2 to create three categories.[37] An additional version, the \"modifiedextended version\", using the more recent cutoff of 2 but including findings from Wells's initialstudies[34][35] were proposed.[38] Most recently, a further study reverted to Wells's earlier use ofa cutoff of 4 points[36] to create only two categories.[39]There are additional prediction rules for PE, such as the Geneva rule. More importantly, the useof any rule is associated with reduction in recurrent thromboembolism.[40]The Wells score:[41]clinically suspected DVT – 3.0 pointsalternative diagnosis is less likely than PE – 3.0 pointstachycardia (heart rate > 100) – 1.5 pointsimmobilization (≥ 3d)/surgery in previous four weeks – 1.5 pointshistory of DVT or PE – 1.5 pointshemoptysis – 1.0 pointsmalignancy (with treatment within six months) or palliative – 1.0 pointsTraditional interpretation[36][37][42]Score >6.0 – High (probability 59% based on pooled data)[32]Score 2.0 to 6.0 – Moderate (probability 29% based on pooled data)[32]Score <2.0 – Low (probability 15% based on pooled data)[32]Probability testing
Alternative interpretation[36][39]Score > 4 – PE likely. Consider diagnostic imaging.Score 4 or less – PE unlikely. Consider D-dimer to rule out PE.Recommendations for a diagnostic algorithm were published by the PIOPED investigators;however, these recommendations do not reflect research using 64 slice MDCT.[32] Theseinvestigators recommended:Low clinical probability. If negative D-dimer, PE is excluded. If positive D-dimer, obtain MDCTand base treatment on results.Moderate clinical probability. If negative D-dimer, PE is excluded. However, the authors werenot concerned that a negative MDCT with negative D-dimer in this setting has a 5%probability of being false. Presumably, the 5% error rate will fall as 64 slice MDCT is morecommonly used. If positive D-dimer, obtain MDCT and base treatment on results.High clinical probability. Proceed to MDCT. If positive, treat, if negative, more tests areneeded to exclude PE. A D-dimer of less than 750 ug/L does not rule out PE in those whoare at high risk.[43]The pulmonary embolism rule-out criteria (PERC) helps assess people in whom pulmonaryembolism is suspected, but unlikely. Unlike the Wells score and Geneva score, which are clinicalprediction rules intended to risk stratify people with suspected PE, the PERC rule is designed torule out the risk of PE in people when the physician has already stratified them into a low-riskcategory.[44][42]People in this low risk category without any of these criteria may undergo no further testing forPE: low oxygen saturations – Sa <95%, unilateral leg swelling, coughing up blood, prior DVTO 2or PE, recent surgery or trauma, age >50, hormone use, fast heart rate. The rationale behind thisdecision is that further testing (specifically CT angiogram of the chest) may cause more harm(from radiation exposure and contrast dye) than the risk of PE.[45] The PERC rule has asensitivity of 97.4% and specificity of 21.9% with a false negative rate of 1.0% (16/1666).[44]In people with a low or moderate suspicion of PE, a normal D-dimer level (shown in a blood test)is enough to exclude the possibility of thrombotic PE, with a three-month risk ofthromboembolic events being 0.14%.[46] D-dimer is highly sensitive but not specific (specificityaround 50%). In other words, a positive D-dimer is not synonymous with PE, but a negative D-dimer is, with a good degree of certainty, an indication of absence of a PE.[47] A low pretestprobability is also valuable in ruling out PE.[48] The typical cut off is 500 μg/L, although thisvaries based on the assay.[49] However, in those over the age of 50, changing the cut-off value tothe person's age multiplied by 10 μg/L (accounting for assay which has been used) isrecommended as it decreases the number of falsely positive tests without missing any additionalcases of PE.[30][49][50]When a PE is being suspected, several blood tests are done in order to exclude importantsecondary causes of PE. This includes a full blood count, clotting status (PT, aPTT, TT), andsome screening tests (erythrocyte sedimentation rate, kidney function, liver enzymes,Pulmonary embolism rule-out criteriaBlood tests
electrolytes). If one of these is abnormal, further investigations might be warranted to theissue.[51]Troponin levels are increased in between 16 and 47% with pulmonary embolism.[52]In typical people who are not known to be at high risk of PE, imaging is helpful to confirm orexclude a diagnosis of PE after simpler first-line tests are used.[29][32][53] Medical societiesrecommend tests such as the D-dimer to first provide supporting evidence for the need forimaging, and imaging would be done if other tests confirmed a moderate or high probability offinding evidence to support a diagnosis of PE.[32][53]CT pulmonary angiography is the recommended first line diagnostic imaging test in mostpeople.[54]Ultrasound of the legs can confirm the presence of a PE but cannot rule it out.[55]CT pulmonary angiography (CTPA) is a pulmonary angiogram obtained using computedtomography (CT) with radiocontrast rather than right heart catheterization. Its advantages arethat it is accurate, it is non-invasive, it is more often available, and it may identifying other lungdisorders in case there is no pulmonary embolism. The accuracy and non-invasive nature ofCTPA also make it advantageous for people who are pregnant.[56]ImagingCT pulmonary angiography
On CT scan, pulmonary emboli Segmental and subsegmentalcan be classified according to pulmonary emboli on both sidesthe level along the arterial tree.CT pulmonary angiography Pulmonary embolism (whiteshowing a \"saddle embolus\" at arrow) that has been long-the bifurcation of the main standing and has caused a lungpulmonary artery and thrombus infarction (black arrow) seen asburden in the lobar arteries on a reverse halo sign.both sides.Assessing the accuracy of CT pulmonary angiography is hindered by the rapid changes in thenumber of rows of detectors available in multidetector CT (MDCT) machines.[57] According to acohort study, single-slice spiral CT may help diagnose detection among people with suspectedpulmonary embolism.[58] In this study, the sensitivity was 69% and specificity was 84%. In thisstudy which had a prevalence of detection was 32%, the positive predictive value of 67.0% andnegative predictive value of 85.2%. However, this study's results may be biased due to possibleincorporation bias, since the CT scan was the final diagnostic tool in people with pulmonaryembolism. The authors noted that a negative single slice CT scan is insufficient to rule outpulmonary embolism on its own. A separate study with a mixture of 4 slice and 16 slice scannersreported a sensitivity of 83% and a specificity of 96%, which means that it is a good test for rulingout a pulmonary embolism if it is not seen on imaging and that it is very good at confirming apulmonary embolism is present if it is seen. This study noted that additional testing is necessarywhen the clinical probability is inconsistent with the imaging results.[59] CTPA is non-inferior toVQ scanning, and identifies more emboli (without necessarily improving the outcome) comparedto VQ scanning.[60]Ventilation/perfusion scan
Ventilation-perfusion scintigraphy (A) After inhalation of 20 mCi ofXenon-133 gas, scintigraphicimages were obtained in theposterior projection, showinguniform ventilation to lungs. (B) After intravenous injection of 4mCi of Technetium-99m-labeledalbumin, scintigraphic imagesshown here in the posteriorprojection. This and other viewsshowed decreased activity inmultiple regions.A ventilation/perfusion scan (or V/Q scan or lungscintigraphy) shows that some areas of the lung are beingventilated but not perfused with blood (due to obstruction bya clot).[17] This type of examination is as accurate asmultislice CT, but is less used, due to the greater availabilityof CT technology. It is particularly useful in people who havean allergy to iodinated contrast, impaired kidney function, orare pregnant (due to its lower radiation exposure ascompared to CT).[61][62][63] The test can be performed withplanar two-dimensional imaging, or single photon emissioncomputed tomography (SPECT) which enables three-dimensional imaging.[54] Hybrid devices combining SPECTand CT (SPECT/CT) further enable anatomiccharacterization of any abnormality.[64]Tests that are frequently done that are not sensitive for PE,but can be diagnostic.Chest X-rays are often done on people with shortness of breath to help rule-out othercauses, such as congestive heart failure and rib fracture. Chest X-rays in PE are rarelynormal,[65] but usually lack signs that suggest the diagnosis of PE (for example, Westermarksign, Hampton's hump).Ultrasonography of the legs, also known as leg doppler, in search of deep venous thrombosis(DVT). The presence of DVT, as shown on ultrasonography of the legs, is in itself enough towarrant anticoagulation, without requiring the V/Q or spiral CT scans (because of the strongassociation between DVT and PE). This may be a valid approach in pregnancy, in which theother modalities would increase the risk of birth defects in the unborn child. However, anegative scan does not rule out PE, and low-radiation dose scanning may be required if themother is deemed at high risk of having a pulmonary embolism. The main use ofultrasonography of the legs is therefore in those with clinical symptoms suggestive of deepvein thrombosis.[63]Historically, the gold standard for diagnosis was pulmonary angiography by fluoroscopy, but thishas fallen into disuse with the increased availability of non-invasive techniques that offer similardiagnostic accuracy.[66]The primary use of the ECG is to rule out other causes of chest pain.[67] An electrocardiogram(ECG) is routinely done on people with chest pain to quickly diagnose myocardial infarctions(heart attacks), an important differential diagnosis in an individual with chest pain. Whilecertain ECG changes may occur with PE, none are specific enough to confirm or sensitive enoughto rule out the diagnosis.[67] An ECG may show signs of right heart strain or acute cor pulmonalein cases of large PEs – the classic signs are a large S wave in lead I, a large Q wave in lead III, andan inverted T wave in lead III (S1Q3T3), which occurs in 12–50% of people with the diagnosis,yet also occurs in 12% without the diagnosis.[68][69]Low probability diagnostic tests/non-diagnostic testsFluoroscopic pulmonary angiographyElectrocardiogram
Selective pulmonary angiogramrevealing clot (labeled A) causing acentral obstruction in the left mainpulmonary artery. ECG tracingshown at the bottom.Electrocardiogram of a person with pulmonaryembolism, showing sinus tachycardia ofapproximately 100 beats per minute, large Swave in Lead I, moderate Q wave in Lead III,inverted T wave in Lead III, and inverted T wavesin leads V1 and V3.This is occasionally present (occurring in up to 20% ofpeople), but may also occur in other acute lung conditions,and, therefore, has limited diagnostic value. The mostcommonly seen signs in the ECG are sinus tachycardia, rightaxis deviation, and right bundle branch block.[70] Sinustachycardia, however, is still only found in 8–69% of peoplewith PE.[71]ECG findings associated with pulmonary emboli may suggestworse prognosis since the six findings identified with RVstrain on ECG (heart rate > 100 beats per minute, S1Q3T3,inverted T waves in leads V1-V4, ST elevation in aVR,complete right bundle branch block, and atrial fibrillation)are associated with increased risk of circulatory shock anddeath.[72]Cases with inverted T in leads V1-3 are suspected with PE orinferior myocardial infarction. PE cases show inverted Twaves in leads II and aV , but inferior myocardial infarctionFcases do not show inverted T waves in II and aV .F[73]In massive and submassive PE, dysfunction ofthe right side of the heart may be seen onechocardiography, an indication that thepulmonary artery is severely obstructed and theright ventricle, a low-pressure pump, is unable tomatch the pressure. Some studies (see below)suggest that this finding may be an indication forthrombolysis. Not every person with a(suspected) pulmonary embolism requires anechocardiogram, but elevations in cardiactroponins or brain natriuretic peptide mayindicate heart strain and warrant an echocardiogram,[74] and be important in prognosis.[75]The specific appearance of the right ventricle on echocardiography is referred to as theMcConnell's sign. This is the finding of akinesia of the mid-free wall but a normal motion of theapex. This phenomenon has a 77% sensitivity and a 94% specificity for the diagnosis of acutepulmonary embolism in the setting of right ventricular dysfunction.[76]Echocardiography
Ultrasound of the Ultrasound of theheart showing signs heart showing signsof PE[77]of PE[77]Pulmonary embolism may be preventable in those with risk factors. People admitted to hospitalmay receive preventative medication, including unfractionated heparin, low molecular weightheparin (LMWH), or fondaparinux, and anti-thrombosis stockings to reduce the risk of a DVT inthe leg that could dislodge and migrate to the lungs.[78]Following the completion of anticoagulation in those with prior PE, long-term aspirin is useful toprevent recurrence.[5]Anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such asoxygen or analgesia, may be required. People are often admitted to hospital in the early stages oftreatment, and tend to remain under inpatient care until the INR has reached therapeutic levels(if warfarin is used). Increasingly, however, low-risk cases are managed at home in a fashionalready common in the treatment of DVT.[5][79] Evidence to support one approach versus theother is weak.[80]Anticoagulant therapy is the mainstay of treatment. For many years, vitamin K antagonists(warfarin or less commonly acenocoumarol or phenprocoumon) have been the cornerstone. Asvitamin K antagonists do not act immediately, initial treatment is with rapidly acting injectableanticoagulants: unfractionated heparin (UFH), low molecular weight heparin (LMWH), orfondaparinux, while oral vitamin K antagonists are initiated and titrated (usually as part ofinpatient hospital care) to the international normalized ratio, a test that determines the dose.[5]In terms of injectable treatments, LMWH may reduce bleeding among people with pulmonaryembolism as compared to UFH.[81] According to the same review, LMWH reduced the incidenceof recurrent thrombotic complications and reduced thrombus size when compared to heparin.There was no difference in overall mortality between participants treated with LMWH and thosetreated with unfractionated heparin.[81] Vitamin K antagonists require frequent dose adjustmentand monitoring of the international normalized ratio (INR). In PE, INRs between 2.0 and 3.0 aregenerally considered ideal.[5] If another episode of PE occurs under warfarin treatment, the INRwindow may be increased to e.g. 2.5–3.5 (unless there are contraindications) or anticoagulationmay be changed to a different anticoagulant e.g. LMWH.[5]PreventionTreatmentAnticoagulation
Used inferior vena cava filter.In recent years, many anticoagulants have been introduced that offer similar to warfarin butwithout a need for titration to the INR. Known as the directly acting oral anticoagulants, thesetreatments are now preferred over vitamin K antagonists by American professional guidelines.[5]Two of these (rivaroxaban and apixaban) do not require initial heparin or fondaparinuxtreatment, whereas dabigatran and edoxaban do.[5] A Cochrane review found that there is noevidence of a difference between oral DTIs (dabigatran, rivaroxaban, edoxaban, apixaban) andstandard anticoagulation in the prevention of recurrent pulmonary embolism.[82]In people with cancer who develop pulmonary embolism, therapy with a course of LMWH isfavored over warfarin or other oral anticoagulants.[5][83] Similarly, pregnant women are treatedwith low molecular weight heparin until after delivery to avoid the known teratogenic effects ofwarfarin, especially in the early stages of pregnancy, but it can be used while breastfeeding.[63]Anticoagulation therapy is usually continued for 3–6 months, or \"lifelong\" if there have beenprevious DVTs or PEs, or none of the usual transient risk factors is present.[5][83] In thosewithout a known cause that can be reversed 2 years of treatment may be better than 6months.[84] For those with small PEs (known as subsegmental PEs) the effects of anticoagulationis unknown as it has not been properly studied as of 2020.[85]Massive PE causing hemodynamic instability (shock and/or low blood pressure, defined as asystolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for >15 min if not caused bynew-onset arrhythmia, hypovolemia or sepsis) is an indication for thrombolysis, the enzymaticdestruction of the clot with medication. In this situation, it is the best available treatment inthose without contraindications and is supported by clinical guidelines.[33][83][86] It is alsorecommended in those in cardiac arrest with a known PE.[87] Catheter-directed thrombolysis(CDT) is a new technique found to be relatively safe and effective for massive PEs. This involvesaccessing the venous system by placing a catheter into a vein in the groin and guiding it throughthe veins by using fluoroscopic imaging until it is located next to the PE in the lung circulation.Medication that breaks up blood clots is released through the catheter so that its highestconcentration is directly next to the pulmonary embolus. CDT is performed by interventionalradiologists or vascular surgeons, and in medical centers that offer CDT, it may be offered as afirst-line treatment.[88]Catheter-based ultrasound-assisted thrombolysis is beinginvestigated.[89]The use of thrombolysis in non-massive PEs is still debated.[90][91] Some have found that thetreatment decreases the risk of death and increases the risk of bleeding including intracranialhemorrhage.[92] Others have found no decrease in the risk of death.[91]There are two situations when an inferior vena cava filter isconsidered advantageous, and those are if anticoagulanttherapy is contraindicated (e.g. shortly after a majoroperation), or a person has a pulmonary embolus in spite ofbeing anticoagulated.[83] In these instances, it may beimplanted to prevent new or existing DVTs from entering thepulmonary artery and combining with an existingblockage.[83] In spite of the device's theoretical advantage ofpreventing pulmonary emboli, there is a lack of evidenceThrombolysisInferior vena cava filter
supporting its effectiveness.[93]Inferior vena cava filters should be removed as soon as it becomes safe to start usinganticoagulation.[83] Although modern filters are meant to be retrievable, complications mayprevent some from being removed. The long-term safety profile of permanently leaving a filterinside the body is not known.[93]Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommonand has largely been abandoned because of poor long-term outcomes. However, recently, it hasgone through a resurgence with the revision of the surgical technique and is thought to benefitcertain people.[94] Chronic pulmonary embolism leading to pulmonary hypertension (known aschronic thromboembolic hypertension) is treated with a surgical procedure known as apulmonary thromboendarterectomy.[95]There are roughly 10 million cases of pulmonary embolisms per year.[23] In the United States,pulmonary embolisms are the primary cause of at least 10,000 to 12,000 deaths per year and acontributing cause in at least 30,000 to 40,000 deaths per year.[9] True incidence involvingpulmonary embolisms is unknown because they often go undiagnosed or unnoticed untilautopsy.[23] From 1993 to 2012, there have been an increased number of admissions in hospitalsdue to pulmonary embolisms, jumping from 23 cases per 100,000 people to 65 cases per100,000 people.[23] Despite this increase, there has been a decrease in mortality during thatsame time period due to medical advances that have occurred.[23]Venous thromboembolism (VTE), a common risk factor, is present at much higher rates in thoseover the age of 70 (three times higher compared to those aged 45 to 69).[23] This is likely due tothere being a generally lower level of activity among the elderly, resulting in higher rates ofimmobility and obesity.[23] VTE has a large, and continuously rising, case fatality rate.[23] Thisrate is roughly 10% after 30 days, 15% after three months and up to 20% after one year.[23]Pulmonary embolisms alone (when resulting in hospitalizations) have a case fatality rate ofabout 5% to 10% so VTE can play a large factor in the severity of the embolisms.[23]When looking at all cases, the rate of fatal pulmonary emboli has declined from 6% to 2% overthe last 25 years in the United States.[96] In Europe, an average of approximately 40,000 deathsper year with pulmonary embolism as the primary cause were reported between 2013 and 2015,a conservative estimate because of potential underdiagnosis.[10]Less than 5 to 10% of symptomatic PEs are fatal within the first hour of symptoms.[33][87]There are several markers used for risk stratification and these are also independent predictorsof adverse outcomes. These include hypotension, cardiogenic shock, syncope, evidence of rightheart dysfunction, and elevated cardiac enzymes.[33] Some ECG changes including S1Q3T3 alsocorrelate with a worse short-term prognosis.[21] There have been other patient-related factorssuch as COPD and chronic heart failure thought to also play a role in prognosis.[33]SurgeryEpidemiologyPrognosis
Large saddle embolus seen in thepulmonary artery (white arrows).Prognosis depends on the amount of lung that is affectedand on the co-existence of other medical conditions; chronicembolisation to the lung can lead to pulmonaryhypertension. After a massive PE, the embolus must beresolved somehow if the patient is to survive. In thromboticPE, the blood clot may be broken down by fibrinolysis, or itmay be organized and recanalized so that a new channelforms through the clot. Blood flow is restored most rapidlyin the first day or two after a PE.[97] Improvement slowsthereafter and some deficits may be permanent. There iscontroversy over whether small subsegmental PEs needtreatment at all[98] and some evidence exists that patientswith subsegmental PEs may do well without treatment.[59][99]Once anticoagulation is stopped, the risk of a fatal pulmonary embolism is 0.5% per year.[100]Mortality from untreated PEs was said to be 26%. This figure comes from a trial published in1960 by Barrit and Jordan, which compared anticoagulation against placebo for the managementof PE. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957.[101] Thisstudy is the only placebo-controlled trial ever to examine the place of anticoagulants in thetreatment of PE, the results of which were so convincing that the trial has never been repeated asto do so would be considered unethical. That said, the reported mortality rate of 26% in theplacebo group is probably an overstatement, given that the technology of the day may havedetected only severe PEs.[102]The PESI and sPESI scoring tools can estimate mortality of patients. The Geneva prediction rulesand Wells criteria are used to calculate a pre-test probability of patients to predict who has apulmonary embolism. These scores are tools to be used with clinical judgment in decidingdiagnostic testing and types of therapy.[103] The PESI algorithm comprises 11 routinely availableclinical variables.[104] It puts the subjects into one of five classes (I–V), with 30-day mortalityranging from 1.1% to 24.5%. Those in classes I and II are low-risk and those in classes III–V arehigh-risk.[104]1. \"What Are the Signs and Symptoms of Pulmonary Embolism?\" (https://www.nhlbi.nih.gov/health/health-topics/topics/pe/signs). NHLBI. July 1, 2011. Archived (https://web.archive.org/web/20160309014739/https://www.nhlbi.nih.gov/health/health-topics/topics/pe/signs) from theoriginal on 9 March 2016. Retrieved 12 March 2016.2. Goldhaber SZ (2005). \"Pulmonary thromboembolism\". In Kasper DL, Braunwald E, Fauci AS,et al. (eds.). Harrison's Principles of Internal Medicine (16th ed.). New York: McGraw-Hill.pp. 1561–65. ISBN 978-0-07-139140-5.3. \"Who Is at Risk for Pulmonary Embolism?\" (https://www.nhlbi.nih.gov/health/health-topics/topics/pe/atrisk). NHLBI. July 1, 2011. Archived (https://web.archive.org/web/20160215115545/http://www.nhlbi.nih.gov/health/health-topics/topics/pe/atrisk) from the original on 15 February2016. Retrieved 12 March 2016.4. \"How Is Pulmonary Embolism Diagnosed?\" (https://www.nhlbi.nih.gov/health/health-topics/topics/pe/diagnosis). NHLBI. July 1, 2011. Archived (https://web.archive.org/web/20160407071108/http://www.nhlbi.nih.gov/health/health-topics/topics/pe/diagnosis) from the original on 7April 2016. Retrieved 12 March 2016.Predicting mortalityReferences
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Classification ICD-10: I26 (https://icd.who.int/browse10/2019/en#/I26)· ICD-9-CM: 415.1Pulmonary embolism (https://curlie.org/Health/Conditions_and_Diseases/Cardiovascular_Disorders/Vascular_Disorders/Thrombosis/) at CurlieWells criteria for pulmonary embolism online calculator (http://www.mdcalc.com/wells-criteria-pulmonary-embolism-p95. Madani, Michael M. (2016). \"50. Pulmonary Thromboendarterectomy\" (https://books.google.com/books?id=pgzYCwAAQBAJ&q=Pulmonary+thromboendarterectomy+pte+pea&pg=PA541). In Peacock, Andrew J.; Naeije, Robert; Rubin, Lewis J. (eds.). Pulmonary Circulation:Diseases and Their Treatment, Fourth Edition. CRC Press. p. 541. ISBN 978-1-4987-1991-9.96. Kumar V, Abbas AK, Fausto N, Mitchell RN (2010). Basic Pathology. New Delhi: Elsevier.p. 98. ISBN 978-81-312-1036-9.97. Walker RH, Goodwin J, Jackson JA (October 1970). \"Resolution of pulmonary embolism\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1819885). British Medical Journal. (5728):4135–39. doi 10.1136/bmj.4.5728.135 (https://doi.org/10.1136%2Fbmj.4.5728.135):.PMC 1819885 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1819885) PMID 5475816 (htt. ps://pubmed.ncbi.nlm.nih.gov/5475816).98. Le Gal G, Righini M, Parent F, van Strijen M, Couturaud F (April 2006). \"Diagnosis andmanagement of subsegmental pulmonary embolism\". Journal of Thrombosis andHaemostasis. (4): 724–31. 4doi 10.1111/j.1538-7836.2006.01819.x (https://doi.org/10.1111%:2Fj.1538-7836.2006.01819.x) PMID 16634736 (https://pubmed.ncbi.nlm.nih.gov/16634736). .S2CID 20515117 (https://api.semanticscholar.org/CorpusID:20515117).99. Perrier A, Bounameaux H (June 2006). \"Accuracy or outcome in suspected pulmonaryembolism\". The New England Journal of Medicine. 354 (22): 2383–85.doi 10.1056/NEJMe068076 (https://doi.org/10.1056%2FNEJMe068076) PMID 16738276 (htt:. ps://pubmed.ncbi.nlm.nih.gov/16738276).100. White RH (October 2008). \"Risk of fatal pulmonary embolism was 0.49 per 100 person-yearsafter discontinuing anticoagulant therapy for venous thromboembolism\". Evidence-BasedMedicine. 13 (5): 154. doi 10.1136/ebm.13.5.154 (https://doi.org/10.1136%2Febm.13.5.154):.PMID 18836122 (https://pubmed.ncbi.nlm.nih.gov/18836122) S2CID 29062377 (https://api.s. emanticscholar.org/CorpusID:29062377).101. Barritt DW, Jordan SC (June 1960). \"Anticoagulant drugs in the treatment of pulmonaryembolism. A controlled trial\". Lancet. (7138): 1309–12. 1doi 10.1016/S0140-6736(60)92299-:6 (https://doi.org/10.1016%2FS0140-6736%2860%2992299-6) PMID 13797091 (https://pub. med.ncbi.nlm.nih.gov/13797091).102. Cugell, D. W.; Buckingham, W. B.; Webster, J. R.; Kettel, L. J. (January 1967). \"Thelimitations of laboratory methods in the diagnosis of pulmonary embolism\" (https://pubmed.ncbi.nlm.nih.gov/4869238/). The Medical Clinics of North America. 51 (1): 175–184.doi 10.1016/s0025-7125(16)33092-9 (https://doi.org/10.1016%2Fs0025-7125%2816%29330:92-9) ISSN 0025-7125 (https://www.worldcat.org/issn/0025-7125) PMID 4869238 (https://pu. . bmed.ncbi.nlm.nih.gov/4869238).103. Jiménez D, Yusen RD, Otero R, Uresandi F, Nauffal D, Laserna E, et al. (July 2007).\"Prognostic models for selecting patients with acute pulmonary embolism for initial outpatienttherapy\". Chest. 132 (1): 24–30. doi 10.1378/chest.06-2921 (https://doi.org/10.1378%2Fches:t.06-2921) PMID 17625081 (https://pubmed.ncbi.nlm.nih.gov/17625081). .104. Zhou XY, Ben SQ, Chen HL, Ni SS (December 2012). \"The prognostic value of pulmonaryembolism severity index in acute pulmonary embolism: a meta-analysis\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3571977). Respiratory Research. 13 (1): 111. doi 10.1186/1465-:9921-13-111 (https://doi.org/10.1186%2F1465-9921-13-111) PMC 3571977 (https://www.ncb. i.nlm.nih.gov/pmc/articles/PMC3571977) PMID 23210843 (https://pubmed.ncbi.nlm.nih.gov/. 23210843).External linksD
(http://www.icd9data.com/getICD9Code.ashx?icd9=415.1)· MeSH: D011655(https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&term=D011655) ·DiseasesDB:10956 (http://www.diseasesdatabase.com/ddb10956.htm)ExternalresourcesMedlinePlus:000132 (https://www.nlm.nih.gov/medlineplus/ency/article/000132.htm) ·eMedicine:med/1958 (https://emedicine.medscape.com/med/1958-overview) emerg/490(http://www.emedicine.com/emerg/topic490.htm#)radio/582 (http://www.emedicine.com/radio/topic582.htm#) ·Patient UK:Pulmonaryembolism (https://patient.info/doctor/pulmonary-embolism)e/)Clinical prediction website – Wells criteria for pulmonaryembolism (http://www.clinicalprediction.com/wells-score-for-pe/) Media related to Pulmonary embolism at WikimediaCommons\"Pulmonary Embolism\" (https://medlineplus.gov/pulmonaryembolism.html). MedlinePlus. U.S. National Library ofMedicine.Retrieved from \"https://en.wikipedia.org/w/index.php?title=Pulmonary_embolism&oldid=1042054027\"This page was last edited on 3 September 2021, at 00:14 (UTC).Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By usingthis site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the WikimediaFoundation, Inc., a non-profit organization.
PurpuraPetechiae and purpura on the lower limb due tomedication-induced vasculitisSpecialtyDermatology, hematologyPurpuraPurpura (/ p rpj r / ) is a condition of red orˈ ɜːʊə ə[1]purple discolored spots on the skin that do notblanch on applying pressure. The spots are causedby bleeding underneath the skin secondary toplatelet disorders, vascular disorders, coagulationdisorders, or other causes.[2] They measure 3–10 mm,[3] whereas petechiae measure less than3 mm, and ecchymoses greater than 1 cm.[4]Purpura is common with typhus and can bepresent with meningitis caused by meningococcior septicaemia. In particular, meningococcus(Neisseria meningitidis), a Gram-negativediplococcus organism, releases endotoxin when itlyses. Endotoxin activates the Hageman factor(clotting factor XII), which causes disseminatedintravascular coagulation (DIC). The DIC is whatappears as a rash on the affected individual.ClassificationEtymology and pronunciationSee alsoReferencesExternal linksPurpura are a common and nonspecific medical sign; however, the underlying mechanismcommonly involves one of:Platelet disorders (thrombocytopenic purpura)Primary thrombocytopenic purpuraSecondary thrombocytopenic purpuraPost-transfusion purpuraVascular disorders (nonthrombocytopenic purpura)Microvascular injury, as seen in senile (old age) purpura, when blood vessels are moreeasily damagedHypertensive statesDeficient vascular supportVasculitis, as in the case of Henoch–Schönlein purpuraContentsClassification
Coagulation disordersDisseminated intravascular coagulation (DIC)Scurvy (vitamin C deficiency) – defect in collagen synthesis due to lack of hydroxylationof procollagen results in weakened capillary walls and cellsMeningococcemiaClumping fibrillary protein deposits caused by AmyloidosisCocaine use with concomitant use of the one-time chemotherapy drug and now veterinarydeworming agent levamisole can cause purpura of the ears, face, trunk, or extremities,sometimes needing reconstructive surgery. Levamisole is purportedly a common cutting[5]agent.Decomposition of blood vessels including purpura is a symptom of acute radiation poisoningin excess of 2 Grays of radiation exposure. This is an uncommon cause in general, but iscommonly seen in victims of nuclear disaster.Cases of psychogenic purpura are also described in the medical literature,[6] some claimed to bedue to \"autoerythrocyte sensitization\". Other studies[7] suggest the local (cutaneous) activity oftissue plasminogen activator can be increased in psychogenic purpura, leading to substantialamounts of localized plasmin activity, rapid degradation of fibrin clots, and resultant bleeding.Petechial rash is also characteristic of a rickettsial infection.The word purpura (/ p rp r /) comes from Latin ˈ ɜː ɜː əpurpura, \"purple\", which came from ancientGreek πορφύρα. Purpura is a mass noun naming the condition or state, not the name of anindividual spot (thus there is no *pupurum, *purpura or *purpura, *purpurae countdeclension).Bruise, which is a hematoma caused by traumaPetechia, which is a small type of hematoma (<3 mm)Ecchymosis, which is a large type of hematoma (>1 cm)Purpura secondary to clotting disordersPurpura hemorrhagica in horsesPigmented purpuric dermatosisSchamberg disease (progressive pigmentary purpura)1. https://www.lexico.com/en/definition/purpura2. \"UCSF Purpura Module\" (https://web.archive.org/web/20131002064433/http://www.dermatology.ucsf.edu/education_training/140.01ClinicalDermatology/Module.8.Purpura%20Module%20REVISED2.pdf) (PDF). Archived from the original (http://www.dermatology.ucsf.edu/education_training/140.01ClinicalDermatology/Module.8.Purpura%20Module%20REVISED2.pdf)(PDF) on 2013-10-02.3. McKenzie, Shirlyn B. (2014). Clinical Laboratory Hematology. Williams, Joanne Lynne;Landis-Piwowar, Kristin (3rd ed.). Boston. p. 665. ISBN 978-0133076011 OCLC 878098857. (https://www.worldcat.org/oclc/878098857).4. Robbins basic pathology. Kumar, Vinay; Abbas, Abul K.; Aster, Jon C.; Perkins, James A.(10th ed.). Philadelphia, Pennsylvania. 2017-03-28. p. 101. ISBN 978-0323353175.Etymology and pronunciationSee alsoReferences
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