DOCSLIB.ORG

Acute Pulmonary Oedema and Pulmonary Embolism

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Acute Pulmonary Oedema and Pulmonary Embolism AcuteAcute PulmonaryPulmonary OedemaOedema andand PulmonaryPulmonary EmbolismEmbolism Dr Arthur Chun-Wing LAU 劉俊穎劉俊穎 Associate Consultant Department of Intensive Care Pamela Youde Nethersole Eastern Hospital 25 August 2008 PathogenesisPathogenesis 1. PulmonaryPulmonary edemaedema CardiogenicCardiogenic NonNon--cardiogeniccardiogenic (e.g.(e.g. acuteacute lunglung injuryinjury (ALI),(ALI), acuteacute respiratoryrespiratory distressdistress syndromesyndrome (ARDS)(ARDS) 2. PulmonaryPulmonary embolismembolism CardiogenicCardiogenic pulmonarypulmonary edemaedema Normal lung Pulmonary edema CaseCase M/62M/62 C/oC/o progressiveprogressive SOB,SOB, nonnon--productiveproductive cough,cough, lowlow gradergrader feverfever xx 33 daysdays PastPast health:health: CHFCHF 22 yearsyears agoago P/E:P/E: BPBP 95/5595/55 mmHgmmHg，，PP 110110，，TT 37.937.9℃℃,, SpO2SpO2 96%96% inin RARA Chest:Chest: bilateralbilateral ralesrales andand rhonchirhonchi CommonCommon causescauses ofof APO/CHFAPO/CHF Acute Chronic Both Myocardial infarction Coronary artery disease Hypertension Myocarditis Diabetes: systolic and diastolic dysfucntion Dysrhythmias Alcoholic cardiomyopathy Valvular heart disease (esp aortic and mitral) CHFCHF ViciousVicious CycleCycle Low Output Increased Preload Increased Afterload Norepinephrine Increased Salt Vasoconstriction Renal Blood Flow Renin Angiotension I Angiotension II Aldosterone SymptomsSymptoms AnkleAnkle edemaedema SevereSevere resp.resp. distress:distress: orthopneaorthopnea,, dyspneadyspnea,, paroxysmalparoxysmal nocturnalnocturnal dyspnea.dyspnea. SevereSevere apprehension,apprehension, agitation,agitation, confusion,confusion, diaphoresis:diaphoresis: ResultsResults fromfrom sympatheticsympathetic stimulationstimulation SignsSigns Vitals increase in sympathetic discharge to compensate. BP — elevated Pulse rate — elevated to compensate for decreased stroke volume. Respirations — rapid and labored, desaturation and cyanosis Diaphoresis Pulmonary congestion Rales—especially at the bases. Rhonchi—associated with fluid in the larger airways Wheezes Jugular Venous Distention Comes from back pressure building from right heart into venous circulation Ankle edema, congested liver InvestigationsInvestigations ECG:ECG: looklook forfor cardiaccardiac ischaemiaischaemia Echo:Echo: checkcheck cardiaccardiac function,function, valvularvalvular functionfunction BB--typetype NatriureticNatriuretic PeptidePeptide (BNP):(BNP): lowlow levelslevels ofof BNPBNP (<100(<100 pg/ml)pg/ml) makemake aa cardiaccardiac causecause veryvery unlikelyunlikely LeftLeft vsvs RightRight--sideside HFHF LeftLeft--sidedsided isis associatedassociated withwith dyspneadyspnea,, fatigue,fatigue, weakness,weakness, cough,cough, PND,PND, orthopneaorthopnea andand JVDJVD RightRight--sidedsided isis associatedassociated withwith peripheralperipheral edema,edema, JVD,JVD, RUQRUQ pain,pain, hepatojugularhepatojugular reflexreflex SystolicSystolic vsvs DiastolicDiastolic HFHF Systolic HF impaired contractility leads to increased cardiac volumes and pressure, and afterload sensitivity With stress, failure to improve cardiac contractility, despite increasing venous return results in increased cardiac pressures, pulmonary congestion and edema Diastolic HF decreased LV compliance and higher atrial pressures results in preload sensitivity Decreased LV compliance necessitates higher atrial pressures to ensure adequate diastolic LV filling TreatmentTreatment 100% O2 by face mask to obtain saturation >95% Airway control and adequate ventilation: NIV or MV Sit up 45 degrees Promotion of rest, Relief of anxiety Diuretics: e.g. lasix 40-80 mg IV Control myocaridal ischaemia: aspirin, thrombolytic agents, nitrate, beta-blocker Vasodilators: nitrates, ACEI, Ca channel blocker Control hypertension: nitrate, ACEI, nitroprusside, Ca channel blockers, hydralazine If hypotensive or need for iontropic support: dopamine 5-10 ug/kg/min, dobutamine, digoxin Treat coexisiting arrhythmia or electrolyte disturbance Morphine use PRN Fluid removal in renal shutdown: haemofiltration, haemodialysis Intraaortic ballon pump LV remodelling: ACEI Facial Nasal Nasal pillow Total face VasodilatorVasodilator DilateDilate bloodblood vesselsvessels OftenOften constrictedconstricted duedue toto activationactivation ofof thethe sympatheticsympathetic nervousnervous systemsystem andand thethe reninrenin-- angiotensinangiotensin--aldosteronealdosterone system.system. CommonCommon ACEACE inhibitorsinhibitors PerindoprilPerindopril LisinoprilLisinopril CaptoprilCaptopril NitratesNitrates DiureticsDiuretics LasixLasix Hydrochlorothiazide(HCTZ)Hydrochlorothiazide(HCTZ) SpironolactoneSpironolactone TheseThese inhibitinhibit reabsorptionreabsorption ofof Na+Na+ intointo thethe kidneyskidneys CalciumCalcium channelchannel blockerblocker UsedUsed toto dilatedilate bloodblood vesselsvessels UsedUsed mostlymostly withwith CHFCHF inin thethe presencepresence ofof ischemiaischemia ExamplesExamples Nifedipine Diltiazem Verapamil Amlodipine Felodipine BetaBeta blockersblockers UsefulUseful byby blockingblocking thethe betabeta--adrengergicadrengergic receptorsreceptors ofof thethe sympatheticsympathetic nervousnervous system,system, thethe heartheart raterate andand forceforce ofof contractilitycontractility areare decreaseddecreased couldcould actuallyactually worsenworsen CHFCHF ExamplesExamples Metoprolol Atenolol Propanolol Amiodarone InotropicInotropic agentsagents DopamineDopamine DobutamineDobutamine DigoxinDigoxin IncreasesIncreases thethe contractilitycontractility ofof thethe heartheart increasingincreasing thethe cardiaccardiac outputoutput PreventPrevent thethe productionproduction ofof thethe chemicalschemicals thatthat causescauses bloodblood vesselsvessels toto narrownarrow ResultingResulting inin bloodblood pressurepressure decreasingdecreasing andand thethe heartheart pumpingpumping easiereasier NonNon cardiogeniccardiogenic pulmonarypulmonary edemaedema CausesCauses ofof nonnon--cardiogeniccardiogenic APOAPO (=(= ALI,ALI, ARDS)ARDS) Inhalation of toxic gases Multiple blood transfusions Severe infection Pulmonary contusion, i.e., Multitrauma, e.g., severe car accident Neurogenic, e.g., subarachnoid hemorrhage Aspiration, e.g., gastric fluid or in case of drowning Certain types of medication Upper airway obstruction Arteriovenous malformation Reexpansion, i.e. post pneumonectomy or large volume thoracentesis Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation Ascent to high altitude occasionally causes high altitude pulmonary edema (HAPE)[2] Cardiogenic pulmonary edema •Enlargement of peribronchial vascualar space •Kerley’s B lines Non- cardiogenic pulmonary edema •E.g. pneumococcal septicaemia •Air-bronchograms •Acute lung injury/acute respiratory distress syndrome TreatmentTreatment VentilatoryVentilatory supportsupport DirectDirect toto underlyingunderlying causecause PulmonaryPulmonary embolismembolism InvestigationsInvestigations 18371837 FirstFirst casecase reportreport ofof PEPE 19221922 DescriptionDescription ofof signssigns atat CXRCXR 19631963 PulmonaryPulmonary angiographyangiography 19641964 LungLung scintigraphyscintigraphy 19921992 SpiralSpiral CTCT CaseCase 1:1: F/80,F/80, WKWK HTHT // IHDIHD // CHFCHF // BronchiectasisBronchiectasis SlippedSlipped andand fell,fell, sustainedsustained ## leftleft NOF.NOF. OTOT postponedpostponed forfor 22 weeksweeks duedue toto anan episodeepisode ofof HAPHAP andand fastfast AF.AF. IntraIntra--opop hypotensionhypotension withwith PEA.PEA. Echo:Echo: GrosslyGrossly dilateddilated RVRV SpiralSpiral CTCT thoraxthorax SpiralSpiral CTCT thoraxthorax FillingFilling defectsdefects inin rightright superiorsuperior // inferiorinferior andand leftleft superiorsuperior PAPA andand subsegmentalsubsegmental branches.branches. ProgressProgress ClexaneClexane (low(low molecularmolecular weightweight heparin)heparin) 60mg60mg Q12HQ12H SC.SC. NotNot forfor thrombolyticthrombolytic // embolectomyembolectomy inin viewview ofof unstableunstable haemodynamicshaemodynamics andand extensiveextensive involvement.involvement. SubsequentSubsequent ARFARF withwith anuriaanuria.. SuccumbSuccumb onon D1D1 ICUICU stay.stay. M/64,M/64, HYKHYK HistoryHistory ofof oldold TBTB withwith rightright lobectomylobectomy.. SlipSlip andand fellfell fromfrom aa flightflight ofof stairsstairs CTCT CC--spine:spine: NoNo fracturefracture butbut cordcord impingementimpingement inin C6/7.C6/7. MRIMRI CC--spine:spine: SpinalSpinal stenosisstenosis atat C4/5.C4/5. HeterogeneousHeterogeneous signalssignals inin prepre // paravertebralparavertebral region,region, couldcould bebe oedemaoedema // haemorrhagehaemorrhage.. RehabilitationRehabilitation AbleAble toto walkwalk wthwth frame.frame. IncreasedIncreased SOBSOB withwith desaturationdesaturation.. DifferenceDifference inin calvescalves circumference.circumference. ECG:ECG: SinusSinus tachycardia.tachycardia. RBBB.RBBB. CXR:CXR: ClearClear lunglung fields.fields. Echo:Echo: DilatedDilated RARA // RVRV withwith paradoxicalparadoxical septalseptal motionmotion andand DD--shapedshaped LVLV duringduring diastole;diastole; TR.TR. ProgressProgress SpiralSpiral CT:CT: FillingFilling defectsdefects inin pulmonarypulmonary trunk,trunk, bilateralbilateral pulmonarypulmonary arteriesarteries andand ththeireir segmentalsegmental branches.branches. EnoxaparinEnoxaparin 60mg60mg Q12HQ12H SCSC ++ warfarinwarfarin.. ThrombolyticsThrombolytics
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]
  • Hepatic Hydrothorax: an Updated Review on a Challenging Disease
    Lung (2019) 197:399–405 https://doi.org/10.1007/s00408-019-00231-6 REVIEW Hepatic Hydrothorax: An Updated Review on a Challenging Disease Toufc Chaaban1 · Nadim Kanj2 · Imad Bou Akl2 Received: 18 February 2019 / Accepted: 27 April 2019 / Published online: 25 May 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract Hepatic hydrothorax is a challenging complication of cirrhosis related to portal hypertension with an incidence of 5–11% and occurs most commonly in patients with decompensated disease. Diagnosis is made through thoracentesis after exclud- ing other causes of transudative efusions. It presents with dyspnea on exertion and it is most commonly right sided. Patho- physiology is mainly related to the direct passage of fuid from the peritoneal cavity through diaphragmatic defects. In this updated literature review, we summarize the diagnosis, clinical presentation, epidemiology and pathophysiology of hepatic hydrothorax, then we discuss a common complication of hepatic hydrothorax, spontaneous bacterial pleuritis, and how to diagnose and treat this condition. Finally, we elaborate all treatment options including chest tube drainage, pleurodesis, surgical intervention, Transjugular Intrahepatic Portosystemic Shunt and the most recent evidence on indwelling pleural catheters, discussing the available data and concluding with management recommendations. Keywords Hepatic hydrothorax · Cirrhosis · Pleural efusion · Thoracentesis Introduction Defnition and Epidemiology Hepatic hydrothorax (HH) is one of the pulmonary com- Hepatic hydrothorax is defned as the accumulation of more plications of cirrhosis along with hepatopulmonary syn- than 500 ml, an arbitrarily chosen number, of transudative drome and portopulmonary hypertension. It shares common pleural efusion in a patient with portal hypertension after pathophysiological pathways with ascites secondary to por- excluding pulmonary, cardiac, renal and other etiologies [4].
    [Show full text]
  • Clinical Management of Severe Acute Respiratory Infections When Novel Coronavirus Is Suspected: What to Do and What Not to Do
    INTERIM GUIDANCE DOCUMENT Clinical management of severe acute respiratory infections when novel coronavirus is suspected: What to do and what not to do Introduction 2 Section 1. Early recognition and management 3 Section 2. Management of severe respiratory distress, hypoxemia and ARDS 6 Section 3. Management of septic shock 8 Section 4. Prevention of complications 9 References 10 Acknowledgements 12 Introduction The emergence of novel coronavirus in 2012 (see http://www.who.int/csr/disease/coronavirus_infections/en/index. html for the latest updates) has presented challenges for clinical management. Pneumonia has been the most common clinical presentation; five patients developed Acute Respira- tory Distress Syndrome (ARDS). Renal failure, pericarditis and disseminated intravascular coagulation (DIC) have also occurred. Our knowledge of the clinical features of coronavirus infection is limited and no virus-specific preven- tion or treatment (e.g. vaccine or antiviral drugs) is available. Thus, this interim guidance document aims to help clinicians with supportive management of patients who have acute respiratory failure and septic shock as a consequence of severe infection. Because other complications have been seen (renal failure, pericarditis, DIC, as above) clinicians should monitor for the development of these and other complications of severe infection and treat them according to local management guidelines. As all confirmed cases reported to date have occurred in adults, this document focuses on the care of adolescents and adults. Paediatric considerations will be added later. This document will be updated as more information becomes available and after the revised Surviving Sepsis Campaign Guidelines are published later this year (1). This document is for clinicians taking care of critically ill patients with severe acute respiratory infec- tion (SARI).
    [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]
  • 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]
  • Treatment of Acute Fibrinous Organizing Pneumonia Following Hematopoietic Cell Transplantation with Etanercept
    OPEN Bone Marrow Transplantation (2017) 52, 141–143 www.nature.com/bmt LETTER TO THE EDITOR Treatment of acute fibrinous organizing pneumonia following hematopoietic cell transplantation with etanercept Bone Marrow Transplantation (2017) 52, 141–143; doi:10.1038/ Computed tomography (CT) of the chest showed rapidly bmt.2016.197; published online 15 August 2016 progressive pulmonary infiltrates (Figure 1a). He was admitted to the inpatient bone marrow transplant floor, started on broad- spectrum antimicrobials, and subsequently underwent broncho- Infectious and non-infectious pulmonary complications are scopy that was non-diagnostic. Over the next 2 days he developed reported in 30–60% of all hematopoietic cell transplant (HCT) worsening hypoxemia requiring transfer to the medical intensive – recipients and result in a high morbidity and mortality.1 3 care unit for hypoxemic respiratory failure. High-dose methyl- Non-infectious pulmonary complications encompass a hetero- prednisolone 125 mg every 6 h was initiated. On day +328 he geneous group of conditions including chronic GvHD, frequently underwent video-assisted thoracoscopic surgery (VATS) and left manifested as bronchiolitis obliterans and cryptogenic organizing upper lobe/left lower lobe wedge resection. pneumonia (COP), pulmonary edema, diffuse alveolar hemorrhage He was extubated on day +329, but remained hypoxic, 1 fi and idiopathic pneumonia syndrome. Acute organizing brinous requiring non-invasive ventilation. On day +331 the pathology fi 3 pneumonia (AFOP) was rst described by Beasley et al. in 2002 as from the wedge resections showed Acute organizing fibrinous a unique histological pattern of acute lung injury that is histologically different from diffuse alveolar damage, eosinophilic pneumonia, bronchiolitis obliterans and COP.
    [Show full text]