Pulmonary embolism laboratory findings: Difference between revisions

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:*[[Coagulation studies]],
:*[[Coagulation studies]],
:*Other screening tests such as [[renal function tests]], [[LFT|liver function tests]] and [[electrolyte|electrolyte]] assessment.  
:*Other screening tests such as [[renal function tests]], [[LFT|liver function tests]] and [[electrolyte|electrolyte]] assessment.  
==Arterial blood gas (ABG)==
*In patients with pulmonary embolism, [[ABG|arterial blood gas]] analysis may reveal:<ref name="pmid2491801">{{cite journal |author=Cvitanic O, Marino PL |title=Improved use of arterial blood gas analysis in suspected pulmonary embolism |journal=[[Chest]] |volume=95 |issue=1 |pages=48–51 |year=1989 |month=January |pmid=2491801 |doi= |url=http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=2491801 |accessdate=2012-04-30}}</ref>
:*[[Hypoxemia]],
:*[[Hypocapnia]],
:*Increased [[alveolar-arterial oxygen difference]] ([[Alveolar-arterial gradient|P(A-a)O2 gradient]]) and
:*[[Respiratory alkalosis]].
*However, the above mentioned [[ABG]] findings are not exclusive for the diagnosis PE. Some variations include:
:*[[Hypercapnia]] in cases of massive PE secondary to circulatory collapse.
:*Normal [[PaO2]] ''(partial pressure of oxygen in arterial blood)'' levels as demonstrated by majority of patients.<ref name="pmid1909617">{{cite journal |author=Stein PD, Terrin ML, Hales CA, Palevsky HI, Saltzman HA, Thompson BT, Weg JG |title=Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease |journal=[[Chest]] |volume=100 |issue=3 |pages=598–603 |year=1991 |month=September |pmid=1909617 |doi= |url=http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=1909617 |accessdate=2012-04-30}}</ref>
:*Normal [[alveolar-arterial oxygen gradient]] may be observed in ~6% of patients.
=====Sensitivity and Specificity=====
In patients with suspected PE, Rodger et al, demonstrated that [[ABG]] analysis did not have sufficient [[negative predictive value]], [[specificity]], or likelihood ratios to be considered useful in the management these patients.<ref name="pmid11112122">{{cite journal |author=Rodger MA, Carrier M, Jones GN, Rasuli P, Raymond F, Djunaedi H, Wells PS |title=Diagnostic value of arterial blood gas measurement in suspected pulmonary embolism |journal=[[American Journal of Respiratory and Critical Care Medicine]] |volume=162 |issue=6 |pages=2105–8 |year=2000 |month=December |pmid=11112122 |doi= |url=http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=11112122 |accessdate=2012-04-30}}</ref> Similar findings were observed by the PIOPED II investigators.<ref name="pmid17145249">{{cite journal |author=Stein PD, Woodard PK, Weg JG, Wakefield TW, Tapson VF, Sostman HD, Sos TA, Quinn DA, Leeper KV, Hull RD, Hales CA, Gottschalk A, Goodman LR, Fowler SE, Buckley JD |title=Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II investigators |journal=[[The American Journal of Medicine]] |volume=119 |issue=12 |pages=1048–55 |year=2006 |month=December |pmid=17145249 |doi=10.1016/j.amjmed.2006.05.060 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(06)00779-0 |accessdate=2012-04-30}}</ref>
==D-dimers==
This is formed by the degradation of fibrin clot. Almost all patients with PE have some endogenous fibrinolysis, and therefore have elevated levels of D-dimer.
* The negative predictive value (when done by ELISA) is 91% – 94% .
* Many other diseases are associated with a mild degree of fibrinolysis, and hence an elevated D-dimer is not specific for pulmonary embolism. Disease with elevated levels of D-dimer are:
**[[Pneumonia]]
**[[Congestive heart failure|Congestive heart failure (CHF)]]
**[[Myocardial infarction|Myocardial infarction (MI)]]
**[[Malignancy]]
D-Dimer levels are elevated in other medical conditions such as:
# Pregnancy
# After surgery
# Hospitalized patient.<ref name="pmid19712840">{{cite journal| author=Bruinstroop E, van de Ree MA, Huisman MV| title=The use of D-dimer in specific clinical conditions: a narrative review. | journal=Eur J Intern Med | year= 2009 | volume= 20 | issue= 5 | pages= 441-6 | pmid=19712840 | doi=10.1016/j.ejim.2008.12.004 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19712840  }} </ref> Thus, most hospitalized patients should not undergo D-dimer testing if PE is suspected.<ref name="pmid20592294">{{cite journal| author=Agnelli G, Becattini C| title=Acute pulmonary embolism. | journal=N Engl J Med | year= 2010 | volume= 363 | issue= 3 | pages= 266-74 | pmid=20592294 | doi=10.1056/NEJMra0907731 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20592294  }} </ref>
Patients who are '''hemodynamically stable''', but have a high clinical probability or those having a high d-dimer level should undergo [[Computed tomography#Multislice CT|multidetector CT]].<ref name="pmid16403929">{{cite journal| author=van Belle A, Büller HR, Huisman MV, Huisman PM, Kaasjager K, Kamphuisen PW et al.| title=Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. | journal=JAMA | year= 2006 | volume= 295 | issue= 2 | pages= 172-9 | pmid=16403929 | doi=10.1001/jama.295.2.172 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16403929  }} </ref> The following table depicts the incidences of thromboembolic events in hemodynamicaly stable patients.
{| border="1"
|+
! Condition !! Incidence of thromboembolic event (%)
|-
| Patients not receiving anticoagulation and with negative CT findings.
| 1.5%<ref name="pmid15858185">{{cite journal| author=Perrier A, Roy PM, Sanchez O, Le Gal G, Meyer G, Gourdier AL et al.|title=Multidetector-row computed tomography in suspected pulmonary embolism. | journal=N Engl J Med | year= 2005 | volume= 352|issue= 17 | pages= 1760-8 | pmid=15858185 | doi=10.1056/NEJMoa042905 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15858185}}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16118905Review in: J Fam Pract. 2005 Aug;54(8):653, 657] </ref><ref name="pmid16403929">{{cite journal| author=van Belle A, Büller HR, Huisman MV, Huisman PM, Kaasjager K, Kamphuisen PW et al.|title=Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. | journal=JAMA | year= 2006 | volume= 295 |issue= 2 | pages= 172-9 | pmid=16403929 | doi=10.1001/jama.295.2.172| pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16403929 }} </ref>
|-
| Patients with High d-dimer level
| 1.5%
|-
| Patients with Normal d-dimer level
| 0.5%<ref name="pmid15858185">{{cite journal| author=Perrier A, Roy PM, Sanchez O, Le Gal G, Meyer G, Gourdier AL et al.|title=Multidetector-row computed tomography in suspected pulmonary embolism. | journal=N Engl J Med | year= 2005 | volume= 352|issue= 17 | pages= 1760-8 | pmid=15858185 | doi=10.1056/NEJMoa042905 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15858185}}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16118905Review in: J Fam Pract. 2005 Aug;54(8):653, 657] </ref>
|}
In '''low-to-moderate''' suspicion of PE, a normal [[D-dimer]] level (shown in a [[blood test]]) is enough to exclude the possibility of thrombotic PE.<ref name="pmid8165626">{{cite journal |author=Bounameaux H, de Moerloose P, Perrier A, Reber G|title=Plasma measurement of D-dimer as diagnostic aid in suspected venous thromboembolism: an overview |journal=Thromb. Haemost.|volume=71 |issue=1 |pages=1-6 |year=1994 |pmid=8165626 |doi=}}</ref> In patients with '''High''' clinical probability, the use of the d-dimer assay is of limited value.<ref name="pmid19620439">{{cite journal| author=Gupta RT, Kakarla RK, Kirshenbaum KJ, Tapson VF| title=D-dimers and efficacy of clinical risk estimation algorithms: sensitivity in evaluation of acute pulmonary embolism. |journal=AJR Am J Roentgenol | year= 2009 | volume= 193 | issue= 2 | pages= 425-30 | pmid=19620439 |doi=10.2214/AJR.08.2186 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19620439 }} </ref>
'''The following flowchart summarize the role of D-dimer''':
{{familytree/start |summary=Use of D-Dimer.}}
{{familytree | | | | GMa | GMa=Patients with suspection of [[Pulmonary embolism]]}}
{{familytree | |,|-|-|^|-|-|-|.| | | }}
{{familytree |JOE| | | | |SIS| | | JOE=Clinically Low or Moderate|SIS=Clinically High}}
{{familytree |,|^|-|.| | | | |!| }}
{{familytree |!| | |!| | | | |!| }}
{{familytree |!| | |ME| | |!|ME=D-Dimer Positive}}
{{familytree |!| | | |!| | | |!| }}
{{familytree |MOM| |!| | | |!| |MOM=D-Dimer Negative|}}
{{familytree | |!| | |!| | | |!| }}
{{familytree |GPa| |ME| |SIS|GPa=No treatment|ME=Further Tests|SIS=Further Tests}}
{{familytree/end}}
A new D-Dimer (DDMR) analyzer has shown to have higher accuracy in excluding patients with non-high clinical pre-test probability.<ref name="pmid22245223">{{cite journal| author=Gosselin RC, Wu JR, Kottke-Marchant K, Peetz D, Christie DJ, Muth H et al.| title=Evaluation of the Stratus® CS Acute Care™ D-dimer assay (DDMR) using the Stratus® CS STAT Fluorometric Analyzer: A prospective multisite study for exclusion of pulmonary embolism and deep vein thrombosis. | journal=Thromb Res | year= 2012 | volume=  | issue=  | pages=  | pmid=22245223 | doi=10.1016/j.thromres.2011.12.015 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22245223  }} </ref>
==Brain natriuretic peptide (BNP)==
In a case-control study of 2213 hemodynamically stable patients with suspected acute PE, BNP was found to have 60% sensitivity and 62% specificity.<ref name="pmid16405522">{{cite journal| author=Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR| title=Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism. | journal=J Thromb Haemost | year= 2006 | volume= 4 | issue= 3 | pages= 552-6 | pmid=16405522 | doi=10.1111/j.1538-7836.2005.01752.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16405522  }} </ref>
BNP levels are typically higher in PE patients as compared to patients without PE; however, certain features limit its usefulness as a diagnostic test:
*Many patients with PE do not have elevated BNP levels.
*There are many alternative causes of an elevated BNP level (proving it to be nonspecific).<ref name="pmid16099151">{{cite journal| author=Kiely DG, Kennedy NS, Pirzada O, Batchelor SA, Struthers AD, Lipworth BJ| title=Elevated levels of natriuretic peptides in patients with pulmonary thromboembolism. | journal=Respir Med | year= 2005 | volume= 99 | issue= 10 | pages= 1286-91 | pmid=16099151 | doi=10.1016/j.rmed.2005.02.029 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16099151  }} </ref>
In hemodynamically stable patients, normal level of BNP and pro-BNP have 100% negative predictive value (NPV) for an adverse outcome.<ref name="pmid20592294">{{cite journal| author=Agnelli G, Becattini C| title=Acute pulmonary embolism. | journal=N Engl J Med | year= 2010 | volume= 363 | issue= 3 | pages= 266-74 | pmid=20592294 | doi=10.1056/NEJMra0907731 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20592294  }} </ref> High level of BNP distinguish patients with pulmonary embolism at higher risk of complicated in-hospital duration and death, when compared with those with low BNP levels. However an isolated increase in BNP or NT-pro-BNP level, do not justify more invasive treatment regimens.<ref name="pmid18556626">{{cite journal| author=Klok FA, Mos IC, Huisman MV| title=Brain-type natriuretic peptide levels in the prediction of adverse outcome in patients with pulmonary embolism: a systematic review and meta-analysis. | journal=Am J Respir Crit Care Med | year= 2008 | volume= 178 | issue= 4 | pages= 425-30 | pmid=18556626 | doi=10.1164/rccm.200803-459OC | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18556626  }} </ref>
==Troponin==
Serum troponin I and troponin T are elevated in approximately thirty to fifty percent of the PE patients.<ref name="pmid12904706">{{cite journal| author=Horlander KT, Leeper KV| title=Troponin levels as a guide to treatment of pulmonary embolism. | journal=Curr Opin Pulm Med | year= 2003 | volume= 9 | issue= 5 | pages= 374-7 | pmid=12904706 | doi= | pmc= | url= }} </ref><ref name="pmid12208803">{{cite journal| author=Konstantinides S, Geibel A, Olschewski M, Kasper W, Hruska N, Jäckle S et al.| title=Importance of cardiac troponins I and T in risk stratification of patients with acute pulmonary embolism. | journal=Circulation | year= 2002 | volume= 106 | issue= 10 | pages= 1263-8 | pmid=12208803 | doi= | pmc= | url= }} </ref> The suspected mechanism is due to acute right heart overload.<ref name="pmid11079669">{{cite journal| author=Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB| title=Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction. | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 5 | pages= 1632-6 | pmid=11079669 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11079669  }} </ref> Troponin elevation is more prolonged in acute MI rather in PE and usually resolve within 40 hours after a PE event.<ref name="pmid11901075">{{cite journal| author=Müller-Bardorff M, Weidtmann B, Giannitsis E, Kurowski V, Katus HA| title=Release kinetics of cardiac troponin T in survivors of confirmed severe pulmonary embolism. | journal=Clin Chem | year= 2002 | volume= 48 | issue= 4 | pages= 673-5 | pmid=11901075 | doi= | pmc= | url= }} </ref> Thus troponins are not useful for diagnosis, but there role in prognostic assessment has been proved in a meta-analysis.<ref name="pmid18094010">{{cite journal| author=Jiménez D, Díaz G, Molina J, Martí D, Del Rey J, García-Rull S et al.| title=Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism. | journal=Eur Respir J | year= 2008 | volume= 31 | issue= 4 | pages= 847-53 | pmid=18094010 | doi=10.1183/09031936.00113307 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18094010  }} </ref>


==References==
==References==

Revision as of 18:53, 30 April 2012

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Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Routine laboratory tests including arterial blood gas analysis are non-specific in patients with acute pulmonary embolism; however, in cases of suspected PE they may be ordered to rule-out secondary causes.

Laboratory tests

  • In patients with suspected pulmonary embolism, routine laboratory tests are ordered to exclude the secondary causes of PE. These tests include:

References

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