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, which include:
- Full blood count,
- clotting status (PT, APTT, TT)
- Some screening tests (erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes).
If one of these is abnormal, further investigations might be warranted.
Electrolyte and Biomarker Studies
Arterial blood gas (ABG)
- Cvitanic and Marino[1] stated, that in patients without prior cardiopulmonary disease, 98% of patients with PE had either an increased Alveolar-arterial oxygen difference(AaDO2) or hypocapnia.
- They suggested, therefore, in a patient without cardiopulmonary disease, the probability of PE is very unlikely (i.e. 2%) if they have a normal AaDO2 and a normal PaCO2.
- Other studies by Stein et.al.[2] have not found ABG to have a high enough sensitivity, specificity, positive or negative predictive value to either diagnose PE or prevent further testing in patients thought to have PE.
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.
- Its negative predictive value, however, 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
In a case-control study[9] of 2213 hemodynamically stable patients with suspected acute PE, BNP was found to have 60 percent sensitivity and 62 percent specificity.
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.