Exacerbations of Chronic Obstructive Pulmonary Disease

8/13/2019 Exacerbations of Chronic Obstructive Pulmonary Disease

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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 knon 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 ith COPD have not yet been clearly assessed.

Some evidence points to the importance of considering PE in patients ho

present ith acute exacerbation of COPD ith no obvious cause.

"hrombolytic therapy is the first#line treatment in patients ith high#risk PE

presenting ith cardiogenic shock and$or persistent arterial hypotension.

%n various study shon that thrombolytic therapy rapidly resolves

thromboembolic obstruction and exerts beneficial effects on

haemodynamic parameters.

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

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!)TROD$CT!O)

Pulmonary embolism is knon 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 airay 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 to clinical presentations of venous

thromboembolism )"E* and share the same predisposing factors. %n most

cases PE is a conse0uence of D"./-mong patients ith proximal D",

about 123 have an associated, usually clinically asymptomatic PE at lung

scan. %n about 423 of patients ith PE, D" can be found in the loer

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

knon.!

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 beteen !+.5 to +6.2 cases $

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!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

beteen 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, as admitted to adam malik

hospital ith shortness of breath since past + years and orsened in one

day ith increase cough fre0uency and productive sputum. 9hee:ing as

found and his activities have been restricted and this time he stay on his

bed ith half sitting potition. ;loody cough as reported since ! day ago

ith pink frothy sputum.


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expiration and high picth hee::ing on both hemithorax. -bdominal and

neurological examinations as normally.

(aboratory %nvestigations finding ' hemoglobin !1.! g$d(, hite

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


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Bigure + ' ECA sinustachicardi

%n emergency departement patient as diagnose ith COPD

exacerbation ith suspected pulmonary embolism and hipertension stage

%%, then patient 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 to

times daily. -fter ! hour the patient condition ere getting orsed ith

orsening of breathlessness, restless and decrease of consciousness.

Patient as consulted to intensif care unit and admitted to %C7 anddeceased after + days extensive care.

During admitted, patient using the ventilator ith high flo

oxygenation and volume control. "he oxygen saturation ith oxymetri

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

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 to clinical presentations of venous

thromboembolism )"E* and share the same predisposing factors. %n most

cases PE is a conse0uence of D". -mong patients ith proximal D",

about 123 have been associated, ith clinically asymptomatic PE at lung

scan.6 %n about 423 of patients ith PE, D" can be found in the loer

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 unknon.

Postmortem studies indicate that the prevalence of Emboli in patients ith

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

knon to predispose to deep venous thrombosis and pulmonary

embolism.

enous thromboembolism as present in !53 of COPD patients

hospitalised due to an exacerbation as a complicating or triggering factor.

-lthough the prevalence of "E as shon to be higher in COPD

exacerbations of unknon aetiology, the "E prevalence found in patients

ith an exacerbation of knon aetiology as also considerable.1

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"able !' Predisposing factors for venous thromboembolism.1

Predisposing factor Patient.

related

Setting.

relatedStrong predisposing factors Fracture (hip or leg)

Hip or knee replacementMajor general surgeryMajor trauma

Spinal cor injury

Moderate predisposing factors !rthroscopic knee surgery

"entral #enous lines"hemotherapy"hronic heart or respiratory $ailureHormone replacement therapyMalignancy%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 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 emboli-

PE 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 knoledge, the prevalence and role of PE have not yet been

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determined precisely in COPD exacerbations. PE may be a more common

comorbid condition of COPD than as previously thought, but the data are

limited and contradictory. - diagnosis of PE could easily be dismissed in

COPD, since the main presenting symptoms of PE overlap ith those of a

COPD exacerbation. Some evidence underline the importance of

considering PE in patients ho ere presented ith acute exacerbation of

COPD ith no obvious cause./,1,= -ccording european society of

cardiology guidline +226, symptoms in someone ith PE is 623

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 ith COPD exacerbations need

to be considered.

-ny association beteen acute infection and embolism is of ma8or

clinical importance due to the high rates of both conditions.!2Evidence for

an association beteen 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.

"hromboemboli may also be triggered by infection#associated systemic

inflammation. Aram#positive infections may be associated ith a more

severe and early inflammatory response. "his may be important ith

regard to find of higher thromboembolism risk estimates for Aram positive

bacterial infections.!2,!!

%n this patient found the sign of infection such as fever and increasethe hite blood count. %st may role the leading cause of exacerbation of

COPD and may closely related to embolism.

Suspected PE must be evaluate ith ade0uate clinical aareness

and non invasive diagnosis approach are aranted by various

combination of clinical evaluation plasma d dimer measurent, loer limb

ultrasonography, $ scintigraphy and the definitive invasive standard

criteria by pulmonary angiography.


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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, hich

according to patient characteristics. "he specificity of D#dimer in

suspected PE decreases steadily ith age and may reach !23 in patients

above 62 years. D#dimer is also more fre0uently elevated in patients ith

cancer, in hospitali:ed patients and during pregnancy. "herefore, the

number of patients ith suspected PE in hom D#dimer must be

measured to exclude PE and deciding hether measuring D#dimer is

orthhile for support clinical 8udgement.!,!/

"able + ' >evised Aeneva score.1

0ariable Point

Predisposing a"tors

-ge 51 years

PreviousD" ao PE

Surgery or Bracture ithin ! month

-ctive malignancy

!

+

+Symptoms

7nilateral loer limb pain


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Pain on loer limb deep vein at palpation

F unilateral oedema

/

Clini"al probability

(o

%ntermediate

apid anticoagulation can only be achieved ith

parenteral anticoagulants, such as intravenous unfractionated heparin,

subcutaneous lo#molecular#eight heparin )(?9


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injection $olloe +y in$usionat the rate o$ 1/ 'kg'h su+seuent oses o$

un$ractionate heparin shoul +eajuste using an acti#ate partial

throm+oplastin time (a&)+ase nomogram to rapily reach an

maintain a& prolongation (+eteen 1-5 an 2-5 times control)

corresponing to therapeutic heparin le#els-5/ "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 molecular eight

heparins should be given ith care in patients ith renal failure.

%ntravenous unfractionated heparin should be the preferred mode of initial

anticoagulation for patients 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 eight#ad8usted doses

ithout monitoring. Several trials compared the efficacy and safety of

subcutaneous (?9< ith those of unfractionated heparin. (?9< as at

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

should be initiated ithout delay in patients ith confirmed PE and those

ith a high or intermediate clinical probability of PE hile the diagnostic

orkup is still ongoing. Except for patients at high risk of bleeding and

those ith severe renal dysfunction, subcutaneous (?9< or fondaparinux

rather then intravenous unfractionated heparin should be considered forinitial 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)

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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 Cespiratory

Bailure. -m L >espir Crit Care ?ed +22!J!5/' +6#=!

4. (ippman ?, Bein -. Pulmonary Embolism in "he Patient ith

Chronic Obstructive Pulmonary Disease' - Diagnostic Dilemma.

Chest !=6! J!' =#/+

6. Stebbings -E(, (im "&. -patient 9ith -cute Exacerbation of COPD9ho 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

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!2.Schmidt ?,

Exacerbations of Chronic Obstructive Pulmonary Disease

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