CASE REPORT Lung Embolism in Patient with Respiratory Failure due to COPD

sudarto, syamsul bihar, noni soeroso Division o !ntensi "are Department o Pulmonology and Respiratory #edi"ine S"hool o #edi"ine $niversitas Sumatera $tara% Adam #ali& 'eneral (ospital #edan

Abstra"t Pulmonary embolism is one of the emergencies pulmonology that should be management immediately. Symptoms of disease is usually accompanied by acute onset of respiratory complains. pulmonary embolism can exacerbate respiratory symptoms such as dyspnea and chest pain, and COPD patients are at a high risk for PE due to a variety of factors including limited mobility, inflammation, and comorbidities, the prevalence of PE during exacerbations is uncertain. Pulmonary embolism is kno n to increase the rate of death from COPD at ! year, but the clinical probability of PE and the value of non invasive tests to rule out the diagnosis in patients present presenting ith COPD have not yet been clearly assessed. ith no obvious cause. ith high#risk PE Some evidence points to the importance of considering PE in patients ho ith acute exacerbation of COPD "hrombolytic therapy is the first#line treatment in patients

ith cardiogenic shock and$or persistent arterial hypotension. obstruction and exerts beneficial effects on

%n various study sho n that thrombolytic therapy rapidly resolves thromboembolic haemodynamic parameters.

&ey ords' (ung embolism, COPD, exacerbation.

1

elderly and steroid usage. but the clinical probability of Pulmonary Embolism )PE* and the value of non invasive tests to rule out the diagnosis in patients ith COPD have not yet been clearly assessed.2 cases $ 2 . -mong the triggering factors of COPD exacerbation.! Pulmonary embolism and COPD exacerbations can lead to a state of respiratory failure. -ccording to the -merican#European Consensus. especially in patients ith more severe COPD. -cute exacerbation rates caused by pulmonary embolus are not exacly kno n. Elderly and immobile patient are highly related to the occurrence of deep vein thrombosis )D." can be found in the lo er limbs if sensitive diagnostic methods are used. venous stasis causes thrombus formation.". smoking. incidence of acute respiratory failure occurs bet een !+. usually clinically asymptomatic PE at lung ith PE. / -mong patients scan. congestive heart failure. %n about 423 of patients ith proximal D. about 123 have an associated. %n most cases PE is a conse0uence of D. -s a result of decreased mobility."*.!. D.+ Exacerbations of COPD are episodes of acute deterioration in respiratory symptoms and accompanied by physiological changes and associated ith increases in air ay and systemic inflammation."E* and share the same predisposing factors.1 "he most common risk factors caused by PE are decreased mobility. .".!)TROD$CT!O) Pulmonary embolism is kno n to increase the rate of death from Chronic Obstructive Pulmonary Disease )COPD* at ! year.5 to +6. Patients hospitalised ith an undetermined cause of exacerbation have very strong common risk factors for development of pulmonary thromboemboli." are t o clinical presentations of venous thromboembolism ). "hese episodes are responsible for considerable morbidity and mortality./ PE and D. the role of PE has not yet been clearly determined.

the management of respiratory failure is very important and can optimally estimate relationship bet een the results of the basic disease management. <e reported symptom of fever history of hipertention as found. and signs of increasing right heart failure may indicate deteriorating conditions caused by pulmonary embolus. hemoptysis. <e no history of diabetic.+. decrease of tactile fremitus on both hemithorax.= oC.5 "he diagnosis of pulmonary embolism is intricate despite extensive literature on the sub8ect and clinical experience.5. no history of anti tuberculosis consumption and orked as a driver of public transport as !52$=2 mm<g. central cyanotic.+ times per minute and all temperature . hospital day bed as admitted to adam malik orsened in one as ith shortness of breath since past + years and ith increase cough fre0uency and productive sputum. cough. pulse and family history ith suffering lung disease not found.!22.heavy smoker man. pursed lips breathing and utili:ation of breathing musle on neck and chest examination sho ed simetrical movement of the chest on the percussion and decreasse breath sound bilaterally and also clubing finger and nicotin staining as found in this patient. . ith pink frothy sputum. hiperresonand 3 . chronic lung disease is often included as a ma8or risk factor in pulmonary embolism.loody cough found and his activities have been restricted and this time he stay on his as reported since ! day ago ithout shivering.222 population per year and deaths from respiratory failure as reported around /23. Chest ith the barrel ith prolong chest form. 7pon Physical Examination. fever. 15 years old. %n addition.ital sing sho ed alert. blood pressure rate as !!5 bites per minute. 9hee:ing ith half sitting potition. . 7nder these conditions.4 CASE REPORT . "his is especially applicable in patients ith Exacerbation Onset of COPD here the increased dyspnea. respiratory rate .

. kalium /. >enal function test found the ureum +. Pa2+ 4/ mm<g.4 mE0$(.+3.24 mg$d( and sodium !+= mE0$(.+=.! g$d(. -rterial blood gas analisys values P< 4. %mpression leucositosis. haematocrit . <CO. platelets !/. -bdominal and hite neurological examinations as normally. blood count !4. hyponatremia. mE0$(.!42$mm. (aboratory %nvestigations finding ' hemoglobin !1. C&?...4 mmol$(.. arterial oxygen saturation =+. PaC2+ 1=.222$mm.=. *+ Des *.3. hypervasculari:ation sinustachicardia.-* Tn #n 'tg Bigure !' sho ed consolidation on both hemithorax 4 . clorida =.+ mmol$(. Chest radiographic )+/ dec and ECA examination ith conclussion +2!+* sho ed consolidation on both hemithorax. D dimer !/22 ng$d(.. and metabolic and ith respiratoric acidosis hillar enlargement. /4. total CO+ 12. !6 @g$(. .6 mm<g.expiration and high picth hee::ing on both hemithorax..E #+. troponin t negative.5 mmol$(. ith mild hipoxemia.5 mg$d( and creatinin 2. -drandom blood glucous !!1 g$d(.

then patient as diagnose ith COPD ith suspected pulmonary embolism and hipertension stage as treated base on a standart treatment according to AO(D guidline for COPD such as salbutamol nebuls and fluticason nebuls ! hour continiously. heparin as anticoagulan and electrolit correction. as consulted to intensif care unit and admitted to %C7 and ith high flo ith oxymetri hich deceased after + days extensive care. -fter ! hour the patient condition Patient orsening of breathlessness. During admitted. anti hipertension. broad spectrum antibiotic. Bor the hipertension.1 mg t o ere getting orsed ith times daily. cardiologic departemen as given captopril !+. steroid intravenous and broad spectrum antibiotic and also anti histamin + )ranitidine 12 mg* as a additional treatment. "he oxygen saturation during treatment did not reach more than =+3. "he medication have been given is nebuls bronchodilator. patient using the ventilator oxygenation and volume control. diureticum. 5 . restless and decrease of consciousness. sistemic corticosteroid. nebuls corticosteroid.Bigure + ' ECA sinustachicardi %n emergency departement patient exacerbation %%.

"E prevalence found in patients ith an exacerbation of kno n aetiology as also considerable.D!SC$SS!O) PE and D. congestive heart failure. . scan."E* and share the same predisposing factors. "he risk factors for Embolism in patients ith COPD include immobility. COPD exacerbations may trigger pulmonary embolic events is plausible as acute infections are kno n to predispose to deep venous thrombosis and pulmonary embolism. the . 1 6 . cigarette smoking. "he fre0uency of embolism in patients admitted to the hospital ith acute exacerbation of COPD is unkno n. exacerbations of unkno n aetiology."E as present in !53 of COPD patients as sho n to be higher in COPD hospitalised due to an exacerbation as a complicating or triggering factor.." can be found in the lo er limbs if sensitive diagnostic methods are used.". -mong patients about 123 have been associated. ith Postmortem studies indicate that the prevalence of Emboli in patients COPD may range from +6 to 1!3.". ith clinically asymptomatic PE at lung ith PE.enous thromboembolism -lthough the prevalence of ." are t o clinical presentations of venous thromboembolism ). there have been a number of reports suggesting that the prevalence of deep venous thrombosis and pulmonary embolism is increased in patients ith COPD exacerbation. D.6 -lthough pulmonary embolism is not thought to predispose to exacerbation.6 %n about 423 of patients ith proximal D. %n most cases PE is a conse0uence of D. underlying lung malignancy and advanced age.1 Pulmonary embolism may precipitate acute exacerbations of COPD.

. . . . . .aricose veins "his patient has been diagnosed Patient. 1 Predisposing factor Strong predisposing factors Fracture (hip or leg) Hip or knee replacement Major general surgery Major trauma Spinal cor injury Moderate predisposing factors !rthroscopic knee surgery "entral #enous lines "hemotherapy "hronic heart or respiratory $ailure Hormone replacement therapy Malignancy %ral contracepti#e therapy &aralytic stroke &regnancy'postpartum &re#ious ()* )hrom+ophilia /ea& predisposing a"tors . . . even leading to death in some and differentiation of PE from other causes of exacerbation may be impossible on any clinical grounds. Erderly ith a history of heavy smoking habit. cholecystectomy* Obesity Pregnancy$antepartum .ed rest . . . . . COPD are a predisposing factor for the occurrence of emboliPE may orsen symptoms in COPD patients. . hypertension and chronic respiratory diseases. related . . . ."able !' Predisposing factors for venous thromboembolism. related Setting. days %mmobility due to sitting )eg prolonged car$air travel* %ncreasing age (aparoscopic surgery )eg. ith COPD exacerbations. . . the prevalence and role of PE have not yet been . . . Despite this idely accepted classical kno ledge. %n these patients there is a risk factor for COPD and also embolism. . . . .

-ny association bet een acute infection and embolism is of ma8or clinical importance due to the high rates of both conditions. %st may role the leading cause of exacerbation of Suspected PE must be evaluate ith ade0uate clinical a areness aranted by various COPD and may closely related to embolism. !=3 syncope and !!3 haemoptysis as ell as tachypnoe. Aram#positive infections may be associated severe and early inflammatory response.". +23 cough.determined precisely in COPD exacerbations.!! %n this patient found the sign of infection such as fever and increase the hite blood count. Some evidence underline the importance of ith acute exacerbation of ith PE is 623 ith no obvious cause.!2. fever and cyanosis. but the data are ith those of a limited and contradictory.diagnosis of PE could easily be dismissed in COPD. 1+3 pleuritic pain.1 %n this case found the symptom of dyspnoe. "his may be important bacterial infections. ./. symptoms in someone dyspnoea.$C scintigraphy and the definitive invasive standard criteria by pulmonary angiography. !2 Evidence for an association bet een acute infection and embolism is limited and no studies have been conducted to examine the magnitude and duration of increased throboembolism risk associated ith various infections. "his phenomenon can not be typical of embolism. since the main presenting symptoms of PE overlap considering PE in patients COPD ho ere presented COPD exacerbation. but the possibility of embolism in patients to be considered. PE may be a more common comorbid condition of COPD than as previously thought. ith a more ith "hromboemboli may also be triggered by infection#associated systemic inflammation. and non invasive diagnosis approach are ith COPD exacerbations need regard to find of higher thromboembolism risk estimates for Aram positive combination of clinical evaluation plasma d dimer measurent.= -ccording european society of cardiology guidline +226. haemoptysis and fever. lo er limb ultrasonography. <igh risk PE is an instant life / .1. tachycardia. . signs of D.

has been investigated extensively in recent years. the hom D#dimer must be measured to exclude PE and deciding hether measuring D#dimer is orth hile for support clinical 8udgement. "he most useful initial test in this situation is echocardiography. "he specificity of D#dimer in ith age and may reach !23 in patients ith above 62 years. E+ E+ E. necrosis. D dimer levels in plasma are not useful for confirming PE.1.1 Plasma D#dimer is a degradation product of cross linked fibrin. "herefore. infection.!/ "able + ' >evised Aeneva score. inflammation. !. hich ill usually sho indirect signs of acute pulmonary hypertension and right ventricular overload if acute PE is the cause of the haemodynamic conse0uences. but it can be one of support other than another clinical evaluation. D#dimer levels are elevated in plasma in the presence of an acute clot because of simultaneous activation of coagulation and fibrinolysis. suspected PE decreases steadily hich according to patient characteristics.threatening situation." ao PE Surgery or Bracture ithin ! month -ctive malignancy Symptoms 7nilateral lo er limb pain <aemoptysis Clini"al sign <eart rate 41#=/ beats$min <eart rate D =1 beats$min Point E! E. D#dimer is also more fre0uently elevated in patients number of patients ith suspected PE in cancer.!+ "he diagnostic yield of D#dimer relies on its specificity. and dissection of the aorta. E1 0 .1 0ariable Predisposing a"tors -ge D 51 years PreviousD.. -nother condition may related for fibrin produce. in hospitali:ed patients and during pregnancy. E+ E. such as cancer.

-nticoagulant treatment should be considered in patients ith suspected PE hile a aiting definitive diagnostic confirmation. subcutaneous lo #molecular# eight heparin )(?9<* or subcutaneous fondaparinux. >apid anticoagulation can only be achieved parenteral anticoagulants. regimen a juste intra#enous un$ractionate heparin is /1 2'kg as a +olus 11 . "he ob8ectives of the initial anticoagulant treatment of PE are to prevent death and recurrent events ith an acceptable rate of ith bleeding complications. ho ever. "hrombolytic therapy should be not used in patients ith lo #risk PE. "here are the intermediate clinical probability to embolism according the geneva scoring. but the diagnostic procedure for embolism use the various combination of clinical evaluation and d dimer measurement.+. /#!2 G!! "his patient sho s the symptom of haemoptisis and heart rate D =/ beats$minute. "his patient sho s increase of serum d dimer level. "hrombolytic therapy is the first#line treatment ith high#risk PE presenting ith cardiogenic shock and$or persistent arterial hypotension. it may be considered in selected patients ith intermediate#risk PE and after through consideration for the posibility of increasing the bleeding risk.1 -nticoagulant treatment plays a pivotal role in the management of patients ith PE.Pain on lo er limb deep vein at palpation F unilateral oedema Clini"al probability (o %ntermediate <igh E/ Total 2#. "hat indicated the risk of embolism may occurs in this patient. "he standart definitive for embolism is must include conducting pulmonary arteriography. the invasive procedure ere not perform in this case. %n various study sho n that thrombolytic therapy rapidly resolves thromboembolic in patients obstruction and exerts beneficial effects on haemodynamic parameters. Bre0uent use of thrombolysis in non#high# risk patients is not recommended. such as intravenous unfractionated heparin. ho ever.

6. Bibrinolytic drugs such as streptokinase in patients not given these limitations associated ith the administration. Except for patients at high risk of bleeding and ith severe renal dysfunction.54/ "he aP"" should be measured /H5 hours after the bolus in8ection and then . anticoagulation ith unfractionated heparin.222iu as anticoagulan for treatment of embolism but no clinically meaningful progress. unfractionated heparin can be replaced by (?9< given subcutaneously at subcutaneous (?9< eight#ad8usted doses as at ithout monitoring."E and at least as safe regarding ma8or bleeding.1. CO)CL$S!O) 11 . (o heparins should be given anticoagulation for patients ith care in patients molecular eight ith renal failure. Several trials compared the efficacy and safety of ith those of unfractionated heparin. subcutaneous (?9< or fondaparinux rather then intravenous unfractionated heparin should be considered for initial treatment.!2 "his patient as given heparin initially !2. %t should be noted that aP"" is not a perfect marker of the intensity of the anticoagulant effect of heparin. (?9< or fondaparinux ithout delay in patients ith confirmed PE and those hile the diagnostic should be initiated ith a high or intermediate clinical probability of PE those orkup is still ongoing. %ntravenous unfractionated heparin should be the preferred mode of initial ith severe renal impairment and for those at high risk of bleeding. (?9< least as efficacious as unfractionated heparin regarding the rate of recurrent . hour after each dose ad8ustment. or once daily hen the target therapeutic dose has been reached. as its anticoagulant effect can be rapidly reversed -5 Bor all other cases of acute PE.injection $ollo3e +y in$usionat the rate o$ 1/ 2'kg'h4 su+se5uent oses o$ un$ractionate heparin shoul +ea juste using an acti#ate partial throm+oplastin time (a&)))6+ase nomogram to rapi ly reach an 2-5 times control) maintain a&)) prolongation (+et3een 1-5 an correspon ing to therapeutic heparin le#els.

. Presence of COPD in patients embolism. embolism and COPD are both conditions can mutually aggravate each other. REFERE)CES 12 . ho ever. history of chronic disease.arious risk factors such as elderly comorbid factor for the occurrence of cardiovascular disorders and ith history of heavy smoking is predisposing factor for the occurrence of emboli. as a chest I#ray sho ed diffuse consolidation in both hemithorax and increased serum levels of D dimer. so intensively monitored patients in the intensive care and got the anticoagulant heparin. "he symptoms of pulmonary embolism can occur simultaneously ith COPD exacerbations. Embolism can be occured in COPD patients. %n emergency unit patients given treatment for COPD exacerbations and anti#hypertensive but his condition continued to deteriorate. Embolism diagnosis based on here there are predisposing factors such ell as from ith a as elderly age. smoking history.<ad reported a patient clinical evaluation be enforced ith pulmonary embolism diagnosed ith COPD exacerbations and hypertension.

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!2. Smeeth (. D# dimer for the exclusion of acute venous thrombosis and pulmonary embolism' a systematic revie . !. Schmidt ?. Patel &C.54'!241H=. Lournal of %nternal ?edicine +2!+J +4!' 526H!6 !!. "homas S. . <orvath#Puho E. Di Nisio ?. "homsen >9. <ubbard >.allance P. Oostdi8k -<. Ahali9-. -nn %ntern ?ed +22/J!/2'16=H52+. Olson >E. -cute %nfection and . Sorensen <"..B. D#Dimer test in cancer patients ith suspected acute pulmonary embolism. &amphuisen P9. >uling out clinically suspected pulmonary embolism by assessment of clinical probability and D#dimer levels' a management study. van der (eur LL et al. !+. L "hromb <aemost +221J. . <ull >D.enous "hromboembolism. Stein PD.=H/+ 14 . Sohne ?. (utisan LA. . >isk of deep vein thrombosis and pulmonary embolism after acute infection in a community setting. "hromb <aemost +22.rant > et al. !/.J6='=4H!2. Cook C. Smeeth (.. (ancet +225J . <all -L.'!+. (eclerc0 ?A.uller <>.an ?ar i8k &?. . &uipers .