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.

!)TROD$CT!O)
Pulmonary embolism is kno n to increase the rate of death from Chronic Obstructive Pulmonary Disease )COPD* at ! year, 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.!,+ 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. "hese episodes are responsible for considerable morbidity and mortality, especially in patients ith more severe COPD. , -mong the triggering factors of COPD exacerbation, the role of PE has not yet been clearly determined. Patients hospitalised ith an undetermined cause of exacerbation have very strong common risk factors for development of pulmonary thromboemboli. Elderly and immobile patient are highly related to the occurrence of deep vein thrombosis )D."*./ PE and D." are t o clinical presentations of venous thromboembolism )."E* and share the same predisposing factors. %n most cases PE is a conse0uence of D.". / -mong patients scan. %n about 423 of patients ith proximal D.", about 123 have an associated, usually clinically asymptomatic PE at lung ith PE, D." can be found in the lo er limbs if sensitive diagnostic methods are used.1 "he most common risk factors caused by PE are decreased mobility, congestive heart failure, smoking, elderly and steroid usage. -s a result of decreased mobility, venous stasis causes thrombus formation. -cute exacerbation rates caused by pulmonary embolus are not exacly kno n.! Pulmonary embolism and COPD exacerbations can lead to a state of respiratory failure. -ccording to the -merican#European Consensus, incidence of acute respiratory failure occurs bet een !+.5 to +6.2 cases $
2

!22.222 population per year and deaths from respiratory failure

as

reported around /23. 7nder these conditions, the management of respiratory failure is very important and can optimally estimate relationship bet een the results of the basic disease management.+,5 "he diagnosis of pulmonary embolism is intricate despite extensive literature on the sub8ect and clinical experience. "his is especially applicable in patients ith Exacerbation Onset of COPD here the increased dyspnea, cough, hemoptysis, fever, and signs of increasing right heart failure may indicate deteriorating conditions caused by pulmonary embolus. %n addition, chronic lung disease is often included as a ma8or risk factor in pulmonary embolism.4

CASE REPORT
- heavy smoker man, 15 years old, 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. 9hee:ing ith half sitting potition. ;loody cough

found and his activities have been restricted and this time he stay on his as reported since ! day ago ithout shivering, ith pink frothy sputum. <e reported symptom of fever history of hipertention as found. <e

no history of diabetic, no history of anti tuberculosis consumption and orked as a driver of public transport as !52$=2 mm<g, pulse and family history ith suffering lung disease not found. .ital sing sho ed alert, blood pressure rate as !!5 bites per minute, respiratory rate ,+ times per minute and all

temperature ,5.= oC. 7pon Physical Examination, central cyanotic, 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. Chest ith the barrel ith prolong chest form, decrease of tactile fremitus on both hemithorax, hiperresonand

expiration and high picth

hee::ing on both hemithorax. -bdominal and hite

neurological examinations as normally. (aboratory %nvestigations finding ' hemoglobin !1.! g$d(, blood count !4.!42$mm,, haematocrit ,=.+3, platelets !/,.222$mm,. -drandom blood glucous !!1 g$d(. >enal function test found the ureum +,,5 mg$d( and creatinin 2,24 mg$d( and sodium !+= mE0$(, kalium /,4 mE0$(, clorida =, mE0$(, D dimer !/22 ng$d(, troponin t negative, C&?; !6 @g$(. -rterial blood gas analisys values P< 4.+=,, PaC2+ 1=.6 mm<g, Pa2+ 4/ mm<g, <CO, /4.5 mmol$(, total CO+ 12.+ mmol$(, ;E #+.4 mmol$(, arterial oxygen saturation =+,,3. %mpression leucositosis, hyponatremia, and metabolic and ith respiratoric acidosis hillar enlargement, ith mild hipoxemia. Chest radiographic )+/ dec and ECA examination ith conclussion

+2!+* sho ed consolidation on both hemithorax, hypervasculari:ation sinustachicardia.

*+ Des *,-*
Tn #n 'tg

Bigure !' sho ed consolidation on both hemithorax

Bigure + ' ECA sinustachicardi %n emergency departement patient exacerbation %%, 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, steroid intravenous and broad spectrum antibiotic and also anti histamin + )ranitidine 12 mg* as a additional treatment. Bor the hipertension, cardiologic departemen as given captopril !+,1 mg t o ere getting orsed ith times daily. -fter ! hour the patient condition Patient

orsening of breathlessness, restless and decrease of consciousness. as consulted to intensif care unit and admitted to %C7 and ith high flo ith oxymetri hich deceased after + days extensive care. During admitted, patient using the ventilator oxygenation and volume control. "he oxygen saturation

during treatment did not reach more than =+3. "he medication

have been given is nebuls bronchodilator, nebuls corticosteroid, sistemic corticosteroid, broad spectrum antibiotic, anti hipertension, diureticum, heparin as anticoagulan and electrolit correction.
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D!SC$SS!O)
PE and D." are t o clinical presentations of venous

thromboembolism )."E* and share the same predisposing factors. %n most cases PE is a conse0uence of D.". -mong patients about 123 have been associated, scan.6 %n about 423 of patients ith proximal D.", ith clinically asymptomatic PE at lung ith PE, D." can be found in the lo er

limbs if sensitive diagnostic methods are used.1 Pulmonary embolism may precipitate acute exacerbations of COPD. "he risk factors for Embolism in patients ith COPD include immobility, congestive heart failure, cigarette smoking, underlying lung malignancy and advanced age. "he fre0uency of embolism in patients admitted to the hospital ith acute exacerbation of COPD is unkno n. ith Postmortem studies indicate that the prevalence of Emboli in patients COPD may range from +6 to 1!3.6 -lthough pulmonary embolism is not thought to predispose to exacerbation, 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. COPD exacerbations may trigger pulmonary embolic events is plausible as acute infections are kno n to predispose to deep venous thrombosis and pulmonary embolism., .enous thromboembolism -lthough the prevalence of ."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. exacerbations of unkno n aetiology, the ."E prevalence found in patients ith an exacerbation of kno n aetiology as also considerable. 1

"able !' Predisposing factors for venous thromboembolism. 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 $ailure Hormone replacement therapy Malignancy %ral contracepti#e therapy &aralytic stroke &regnancy'postpartum &re#ious ()* )hrom+ophilia /ea& predisposing a"tors ;ed rest ., days %mmobility due to sitting )eg prolonged car$air travel* %ncreasing age (aparoscopic surgery )eg. cholecystectomy* Obesity Pregnancy$antepartum .aricose veins "his patient has been diagnosed Patient. related Setting. related
, , , , ,

, , , , , , , , , , ,

, ,

, , , ,

ith COPD exacerbations. %n

these patients there is a risk factor for COPD and also embolism. Erderly ith a history of heavy smoking habit, hypertension and chronic respiratory diseases, COPD are a predisposing factor for the occurrence of emboliPE may orsen symptoms in COPD patients, even leading to death in some and differentiation of PE from other causes of exacerbation may be impossible on any clinical grounds. Despite this idely accepted classical kno ledge, the prevalence and role of PE have not yet been

determined precisely in COPD exacerbations. PE may be a more common comorbid condition of COPD than as previously thought, but the data are ith those of a limited and contradictory. - diagnosis of PE could easily be dismissed in COPD, since the main presenting symptoms of PE overlap considering PE in patients COPD ho ere presented COPD exacerbation. Some evidence underline the importance of ith acute exacerbation of ith PE is 623 ith no obvious cause./,1,= -ccording european society of

cardiology guidline +226, symptoms in someone

dyspnoea, 1+3 pleuritic pain, +23 cough, !=3 syncope and !!3 haemoptysis as ell as tachypnoe, signs of D.", fever and cyanosis.1 %n this case found the symptom of dyspnoe, tachycardia, haemoptysis and fever. "his phenomenon can not be typical of embolism, but the possibility of embolism in patients to be considered. -ny association bet een acute infection and embolism is of ma8or clinical importance due to the high rates of both conditions. !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. ith a more ith "hromboemboli may also be triggered by infection#associated systemic inflammation. Aram#positive infections may be associated severe and early inflammatory response. "his may be important bacterial infections.!2,!! %n this patient found the sign of infection such as fever and increase the hite blood count. %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. 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, lo er limb ultrasonography, .$C scintigraphy and the definitive invasive standard criteria by pulmonary angiography. <igh risk PE is an instant life
/

threatening situation. "he most useful initial test in this situation is echocardiography, hich ill usually sho indirect signs of acute pulmonary hypertension and right ventricular overload if acute PE is the cause of the haemodynamic conse0uences.1 Plasma D#dimer is a degradation product of cross linked fibrin, has been investigated extensively in recent years. D#dimer levels are elevated in plasma in the presence of an acute clot because of simultaneous activation of coagulation and fibrinolysis. -nother condition may related for fibrin produce, such as cancer, inflammation, infection, necrosis, and dissection of the aorta. D dimer levels in plasma are not useful for confirming PE, but it can be one of support other than another clinical evaluation.1,!+ "he diagnostic yield of D#dimer relies on its specificity, suspected PE decreases steadily hich according to patient characteristics. "he specificity of D#dimer in ith age and may reach !23 in patients ith above 62 years. D#dimer is also more fre0uently elevated in patients number of patients ith suspected PE in

cancer, in hospitali:ed patients and during pregnancy. "herefore, the hom D#dimer must be measured to exclude PE and deciding hether measuring D#dimer is

orth hile for support clinical 8udgement. !,,!/ "able + ' >evised Aeneva score.1 0ariable Predisposing a"tors -ge D 51 years PreviousD." 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, E+ E+ E, E+ E, E1
0

Pain on lo er limb deep vein at palpation F unilateral oedema Clini"al probability (o %ntermediate <igh

E/ Total 2#, /#!2 G!!

"his patient sho s the symptom of haemoptisis and heart rate D =/ beats$minute. "here are the intermediate clinical probability to embolism according the geneva scoring. "he standart definitive for embolism is must include conducting pulmonary arteriography, ho ever, the invasive procedure ere not perform in this case, but the diagnostic procedure for embolism use the various combination of clinical evaluation and d dimer measurement. "his patient sho s increase of serum d dimer level. "hat indicated the risk of embolism may occurs in this patient. %n various study sho n that thrombolytic therapy rapidly resolves thromboembolic in patients obstruction and exerts beneficial effects on haemodynamic parameters. "hrombolytic therapy is the first#line treatment ith high#risk PE presenting ith cardiogenic shock and$or persistent arterial hypotension. Bre0uent use of thrombolysis in non#high# risk patients is not recommended, ho ever, it may be considered in selected patients ith intermediate#risk PE and after through consideration for the posibility of increasing the bleeding risk. "hrombolytic therapy should be not used in patients ith lo #risk PE.+,1 -nticoagulant treatment plays a pivotal role in the management of patients ith PE. "he ob8ectives of the initial anticoagulant treatment of PE are to prevent death and recurrent events ith an acceptable rate of ith bleeding complications. >apid anticoagulation can only be achieved

parenteral anticoagulants, such as intravenous unfractionated heparin, subcutaneous lo #molecular# eight heparin )(?9<* or subcutaneous fondaparinux. -nticoagulant treatment should be considered in patients ith suspected PE hile a aiting definitive diagnostic confirmation. regimen a juste intra#enous un$ractionate heparin is /1 2'kg as a +olus
11

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- 54/ "he aP"" should be measured /H5 hours after the bolus in8ection and then , hour after each dose ad8ustment, or once daily hen the target therapeutic dose has been reached. %t should be noted that aP"" is not a perfect marker of the intensity of the anticoagulant effect of heparin. (o heparins should be given anticoagulation for patients ith care in patients molecular eight ith renal failure.

%ntravenous unfractionated heparin should be the preferred mode of initial ith severe renal impairment and for those at high risk of bleeding, as its anticoagulant effect can be rapidly reversed -5 Bor all other cases of acute PE, unfractionated heparin can be replaced by (?9< given subcutaneously at subcutaneous (?9< eight#ad8usted doses as at ithout monitoring. Several trials compared the efficacy and safety of ith those of unfractionated heparin. (?9< least as efficacious as unfractionated heparin regarding the rate of recurrent ."E and at least as safe regarding ma8or bleeding. anticoagulation ith unfractionated 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. Except for patients at high risk of bleeding and ith severe renal dysfunction, subcutaneous (?9< or fondaparinux rather then intravenous unfractionated heparin should be considered for initial treatment.1,6,!2 "his patient as given heparin initially !2.222iu as anticoagulan for treatment of embolism but no clinically meaningful progress. Bibrinolytic drugs such as streptokinase in patients not given these limitations associated ith the administration.

CO)CL$S!O)

11

<ad reported a patient clinical evaluation be enforced

ith pulmonary embolism diagnosed

ith

COPD exacerbations and hypertension. Embolism diagnosis based on here there are predisposing factors such ell as from ith a as elderly age, smoking history, history of chronic disease, as

a chest I#ray sho ed diffuse consolidation in both hemithorax and increased serum levels of D dimer. Presence of COPD in patients embolism. .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. Embolism can be occured in COPD patients, ho ever, embolism and COPD are both conditions can mutually aggravate each other. "he symptoms of pulmonary embolism can occur simultaneously ith COPD exacerbations. %n emergency unit patients given treatment for COPD exacerbations and anti#hypertensive but his condition continued to deteriorate, so intensively monitored patients in the intensive care and got the anticoagulant heparin.

REFERE)CES

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!. Erelel ?, Cuhadaroglu C, Ece ", -rseven O. "he Bre0uency of Deep .enous "hrombosis and Pulmonary Embolus in -cute Exacerbation of Chronic Obstructive Pulmonary Disease. >espiratory ?edicine +22+J =5' 1!1#6 +. (eblond %", ?ar0uette C<, Pere: ", Scherpereel -, Kanetti C,et al. Pulmonary Embolism in Patient ith 7nexplained Exacerbation of Chronic ObstructivePulmonary Disease' Prevalence and >isk Bactors. -nn %ntern ?ed. +225J!//',=2#5
,. 9ed:icha L-, <urst L>. Chronic Obstructive Pulmonary Disease

Exacerbation +224J5+'!2,H/

and>isk

of

Pulmonary

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"horax

/. Aunen <, Aulbas A, Metkin O, <acievliyagil SS. .enous "hromboemboli and Exacerbations of COPD. Eur >espir L +2!2J ,1' !+/,H6 1. "orbicki -, Perrier -, &onstantinides S, -gnelli A, Aalie N, et al. Auidlines on "he Diagnosis and ?anagement of -cute Pulmonary Embolism. European <eart Lournal. +226J +=' ++45H,!1 5. Evans "9, -lbert >&, -ngus DC, ;ion LB, Chiche LD, et al. %nternational Consensue Coferences in %ntensive Care ?edicine' Non %nvasive Positive Pressure .entilation in -cute >espiratory Bailure. -m L >espir Crit Care ?ed +22!J!5/' +6,#=! 4. (ippman ?, Bein -. Pulmonary Embolism in "he Patient Chest !=6! J!' ,=#/+ 6. Stebbings -E(, (im "&. -patient 9ith -cute Exacerbation of COPD 9ho Did Not >espond to Conventional "reatment. Chest !==6J !!/'!41=#5! =. Chatila 9?, "homasho ;?, ?inai O-, Criner AL, ?ake ;L. Comorbidities in Chronic Obstructive Pulmonary Disease. Proc -m "horac Soc +226J 1' 1/=H11 ith Chronic Obstructive Pulmonary Disease' - Diagnostic Dilemma.

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

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