Pulmonary embolism laboratory findings
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editors-in-Chief: Ujjwal Rastogi, MBBS [2]
Overview
Arterial blood gas (ABG) measurements and pulse oximetry have a limited role in diagnosing PE. Also, routine laboratory testing are nonspecific. They include:
- Leukocytosis
- Raised erythrocyte sedimentation rate (ESR)
- Raised serum LDH or AST (SGOT) with a normal serum bilirubin.
Blood tests
When PE is suspected, in order to exclude secondary causes of PE, a number of blood tests are done. These include:
- Full blood count
- Clotting status (prothrombin time (PT), APTT, thrombin time (TT))
- Some screening tests (erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes).
If results are abnormal, further investigations might be warranted.
Electrolyte and Biomarker Studies
Arterial blood gas (ABG)
- A study had shown, that in patients without prior cardiopulmonary disease, 98% of patients with PE had either an increased Alveolar-arterial oxygen difference (AaDO2) or hypocapnia[1].
- In a patient without cardiopulmonary disease, having a normal AaDO2 and a normal PaCO2, the probability of PE is very unlikely (i.e. 2%).
- Other studies have found ABG lacking enough sensitivity, specificity, positive or negative predictive value to either diagnose PE or prevent further testing in patients thought to have PE[2].
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 is 91 – 94% (when done by ELISA).
- Many other diseases, such as:
are also associated with a mild degree of fibrinolysis, and hence an elevated D-dimer is not specific for pulmonary embolism.
D-Dimer levels are also elevated in:
- Pregnancy
- After surgery
- Hospitalized patient[3].
Therefore, most hospitalized patients should not undergo D-dimer testing if PE is suspected[4].
Patients who are hemodynamically stable, but have a high clinical probability or those having a high d-dimer level should undergo multidetector CT[5]. 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%[6][5] |
| Patients with High d-dimer level | 1.5% |
| Patients with Normal d-dimer level | 0.5%[6] |
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[7]. In patients with High clinical probability, the use of the d-dimer assay is of limited value[8].
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 | |||||||||||||||||||||
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.[9]
BNP levels are typically higher in patients with PE 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).[10]
In hemodynamically stable patients, normal level of BNP and pro-BNP have 100% negative predictive value (NPV) for an adverse outcome[4]. 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[11].
Troponin
Serum troponin I and troponin T are elevated in approximately thirty to fifty percent of the PE patients.[12][13] The suspected mechanism is due to acute right heart overload.[14] Troponin elevation is more prolonged in acute MI rather in PE and usually resolve within 40 hours after a PE event.[15] Thus troponins are not useful for diagnosis, but there role in prognostic assessment has been proved in a meta-analysis.[16]
References
- ↑ Cvitanic O, Marino PL (1989). "Improved use of arterial blood gas analysis in suspected pulmonary embolism". Chest. 95 (1): 48–51. PMID 2491801.
- ↑ Stein PD, Woodard PK, Weg JG, Wakefield TW, Tapson VF, Sostman HD; et al. (2006). "Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II investigators". Am J Med. 119 (12): 1048–55. doi:10.1016/j.amjmed.2006.05.060. PMID 17145249.
- ↑ 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.
- ↑ 4.0 4.1 Agnelli G, Becattini C (2010). "Acute pulmonary embolism". N Engl J Med. 363 (3): 266–74. doi:10.1056/NEJMra0907731. PMID 20592294.
- ↑ 5.0 5.1 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.
- ↑ 6.0 6.1 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.
- ↑ 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.