Pulmonary embolism laboratory findings
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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 acute pulmonary embolism, routine laboratory findings are non-specific and include: leukocytosis, elevated ESR with an elevated serum LDH and serum transaminase (especially AST or SGOT). However, serum bilirubin levels are found to be within normal limits.
- In patients with suspected pulmonary embolism, routine laboratory tests are ordered to exclude the secondary causes of PE. These tests include:
- Complete blood count,
- Erythrocyte sedimentation rate,
- Coagulation studies,
- Other screening tests such as renal function tests, liver function tests and electrolyte assessment.
Arterial blood gas (ABG)
- In patients with pulmonary embolism, arterial blood gas analysis may reveal:[1]
- Hypoxemia,
- Hypocapnia,
- Increased alveolar-arterial oxygen difference (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.[2]
- 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.[3] Similar findings were observed by the PIOPED II investigators.[4]
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:
D-Dimer levels are elevated in other medical conditions such as:
- Pregnancy
- After surgery
- Hospitalized patient.[5] Thus, most hospitalized patients should not undergo D-dimer testing if PE is suspected.[6]
Patients who are hemodynamically stable, but have a high clinical probability or those having a high d-dimer level should undergo multidetector CT.[7] The following table depicts the incidences of thromboembolic events in hemodynamicaly stable patients.
| Condition | Incidence of thromboembolic event (%) |
|---|---|
| Patients not receiving anticoagulation and with negative CT findings. | 1.5%[8][7] |
| Patients with High d-dimer level | 1.5% |
| Patients with Normal d-dimer level | 0.5%[8] |
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.[9] In patients with High clinical probability, the use of the d-dimer assay is of limited value.[10]
The following flowchart summarize the role of D-dimer:
| Patients with suspection of Pulmonary embolism | |||||||||||||||||||||||
| Clinically Low or Moderate | Clinically High | ||||||||||||||||||||||
| D-Dimer Positive | |||||||||||||||||||||||
| D-Dimer Negative | |||||||||||||||||||||||
| No treatment | Further Tests | Further Tests | |||||||||||||||||||||
A new D-Dimer (DDMR) analyzer has shown to have higher accuracy in excluding patients with non-high clinical pre-test probability.[11]
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.[12]
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).[13]
In hemodynamically stable patients, normal level of BNP and pro-BNP have 100% negative predictive value (NPV) for an adverse outcome.[6] 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.[14]
Troponin
Serum troponin I and troponin T are elevated in approximately thirty to fifty percent of the PE patients.[15][16] The suspected mechanism is due to acute right heart overload.[17] Troponin elevation is more prolonged in acute MI rather in PE and usually resolve within 40 hours after a PE event.[18] Thus troponins are not useful for diagnosis, but there role in prognostic assessment has been proved in a meta-analysis.[19]
References
- ↑ Cvitanic O, Marino PL (1989). "Improved use of arterial blood gas analysis in suspected pulmonary embolism". Chest. 95 (1): 48–51. PMID 2491801. Retrieved 2012-04-30. Unknown parameter
|month=ignored (help) - ↑ Stein PD, Terrin ML, Hales CA, Palevsky HI, Saltzman HA, Thompson BT, Weg JG (1991). "Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease". Chest. 100 (3): 598–603. PMID 1909617. Retrieved 2012-04-30. Unknown parameter
|month=ignored (help) - ↑ Rodger MA, Carrier M, Jones GN, Rasuli P, Raymond F, Djunaedi H, Wells PS (2000). "Diagnostic value of arterial blood gas measurement in suspected pulmonary embolism". American Journal of Respiratory and Critical Care Medicine. 162 (6): 2105–8. PMID 11112122. Retrieved 2012-04-30. Unknown parameter
|month=ignored (help) - ↑ 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 (2006). "Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II investigators". The American Journal of Medicine. 119 (12): 1048–55. doi:10.1016/j.amjmed.2006.05.060. PMID 17145249. Retrieved 2012-04-30. Unknown parameter
|month=ignored (help) - ↑ Bruinstroop E, van de Ree MA, Huisman MV (2009). "The use of D-dimer in specific clinical conditions: a narrative review". Eur J Intern Med. 20 (5): 441–6. doi:10.1016/j.ejim.2008.12.004. PMID 19712840.
- ↑ 6.0 6.1 Agnelli G, Becattini C (2010). "Acute pulmonary embolism". N Engl J Med. 363 (3): 266–74. doi:10.1056/NEJMra0907731. PMID 20592294.
- ↑ 7.0 7.1 van Belle A, Büller HR, Huisman MV, Huisman PM, Kaasjager K, Kamphuisen PW; et al. (2006). "Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography". JAMA. 295 (2): 172–9. doi:10.1001/jama.295.2.172. PMID 16403929.
- ↑ 8.0 8.1 Perrier A, Roy PM, Sanchez O, Le Gal G, Meyer G, Gourdier AL; et al. (2005). "Multidetector-row computed tomography in suspected pulmonary embolism". N Engl J Med. 352 (17): 1760–8. doi:10.1056/NEJMoa042905. PMID 15858185. in: J Fam Pract. 2005 Aug;54(8):653, 657
- ↑ Bounameaux H, de Moerloose P, Perrier A, Reber G (1994). "Plasma measurement of D-dimer as diagnostic aid in suspected venous thromboembolism: an overview". Thromb. Haemost. 71 (1): 1–6. PMID 8165626.
- ↑ Gupta RT, Kakarla RK, Kirshenbaum KJ, Tapson VF (2009). "D-dimers and efficacy of clinical risk estimation algorithms: sensitivity in evaluation of acute pulmonary embolism". AJR Am J Roentgenol. 193 (2): 425–30. doi:10.2214/AJR.08.2186. PMID 19620439.
- ↑ Gosselin RC, Wu JR, Kottke-Marchant K, Peetz D, Christie DJ, Muth H; et al. (2012). "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". Thromb Res. doi:10.1016/j.thromres.2011.12.015. PMID 22245223.
- ↑ Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR (2006). "Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism". J Thromb Haemost. 4 (3): 552–6. doi:10.1111/j.1538-7836.2005.01752.x. PMID 16405522.
- ↑ Kiely DG, Kennedy NS, Pirzada O, Batchelor SA, Struthers AD, Lipworth BJ (2005). "Elevated levels of natriuretic peptides in patients with pulmonary thromboembolism". Respir Med. 99 (10): 1286–91. doi:10.1016/j.rmed.2005.02.029. PMID 16099151.
- ↑ Klok FA, Mos IC, Huisman MV (2008). "Brain-type natriuretic peptide levels in the prediction of adverse outcome in patients with pulmonary embolism: a systematic review and meta-analysis". Am J Respir Crit Care Med. 178 (4): 425–30. doi:10.1164/rccm.200803-459OC. PMID 18556626.
- ↑ Horlander KT, Leeper KV (2003). "Troponin levels as a guide to treatment of pulmonary embolism". Curr Opin Pulm Med. 9 (5): 374–7. PMID 12904706.
- ↑ Konstantinides S, Geibel A, Olschewski M, Kasper W, Hruska N, Jäckle S; et al. (2002). "Importance of cardiac troponins I and T in risk stratification of patients with acute pulmonary embolism". Circulation. 106 (10): 1263–8. PMID 12208803.
- ↑ Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB (2000). "Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction". J Am Coll Cardiol. 36 (5): 1632–6. PMID 11079669.
- ↑ Müller-Bardorff M, Weidtmann B, Giannitsis E, Kurowski V, Katus HA (2002). "Release kinetics of cardiac troponin T in survivors of confirmed severe pulmonary embolism". Clin Chem. 48 (4): 673–5. PMID 11901075.
- ↑ Jiménez D, Díaz G, Molina J, Martí D, Del Rey J, García-Rull S; et al. (2008). "Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism". Eur Respir J. 31 (4): 847–53. doi:10.1183/09031936.00113307. PMID 18094010.