Atypical or typical, is this the question?

Clinical Scenarios

It is a busy day in your ED:

A 60 y/o female refers a retrosternal pain radiates to right arm that lasts more than 20 minutes. 

A 50 y/o male refers a pressure  in his chest, with tachycardia and sweating.

A 75 y/o female refers a sharp and stabbing pain exacerbates by forceful breathing.

In all cases the ECGs are nondiagnostic.

Do these clinical features help to predict an acute myocardial infarction (AMI)?

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Can we fight against Pulmonary Embolism using the LR’s arrows?

Clinical Scenario

A 80 y/o woman presented to the ED for dyspnoea.

She underwent a knee replacement 2 weeks ago, RR is 24, O2 saturation is 88%. HR is 90, the knee is edematous.

You are going to hunt a pulmonary embolism (PE)

While you phone the radiologist for a thorax CT scan you have an idea:

Can a compression ultrasonography (CUS) helps to avoid a CT?

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Chest X-Ray and aortic dissection

Clinical Scenario 

A 70 yo man come to the ED for restrosternal chest pain and shortness of breath during minimal activity in the last days. He is an ex smoker, with a history of hypertension. On physical examination the patient is not in distress, with a regular blood pressure and regular oximetry. ECG shows no evidence of ischemia. You first think about coronary artery disease, but you also want to exclude an aortic dissection. In Radiology the patient remaine seated and receive an anteroposterior (AP) chest Xray: maximal mediastinal width (MW) is 8,80 cm (the optimal cutoff level is 8,65 cm), no other signs. 

Shall you worry?

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Acute Dyspnoea and Laboratory

It’s a dark night when a red code arrive at the ED by ambulance. 

Paramedics tell you: “called for acute dyspnoea, I think it’s a COPD exacerbation, he is wheezing, I gave him bronchodilators and steroids, but he is worsening”.

He has a history of  COPD and hypertension. 

He presents sweaty, dyspneic, arterial pressure is high (220/110).

Physical examination is normal except for wheezing.

AP Chest x ray shows no signs of congestion. 




What about BNP? 

Conclusion

Natriuretic peptides have a very high negative predictive value that allows us to rule out dyspnoea of cardiogenic origin when values are normal. However, there are several circumstances in which natriuretic peptides may be elevated for other reasons, and data may be confounded. Thus, especially in cases where NT-proBNP levels are only slightly abnormal, the “grey zone”, echographic assessment of pulmonary congestion could help in the management of patients with dyspnoea. 

Moreover, natriuretic peptide analysis is not always available, especially in peripheral emergency departments, as it requires specialised laboratory equipment. If the assay is not available, ULCs may offer a plausible alternative. In patients admitted with acute dyspnoea, pulmonary congestion, sonographically imaged as ULCs, is significantly correlated to NT-proBNP values 

Bibliography 

L. Gargani a, F. Frassi a , G. Soldati b , P. Tesorio c , M. Gheorghiade d , E. Picano a

Ultrasound lung comets for the differential diagnosis of acute cardiogenic dyspnoea: A comparison with natriuretic peptides

European Journal of Heart Failure 10 (2008) 70–77

Anwaruddin S, Lloyd-Jones DM, Baggish A, et al.

Renal function, con- gestive heart failure, and amino-terminal pro-brain natriuretic peptide measurement: results from the ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) Study. 

J Am Coll Cardiol 2006;47:91–7.

see also...clinical x ray ultrasound

Ilenia Spallino

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Acute dyspnoea and Lung Ultrasound

It’s a dark night when a red code arrive at the ED by ambulance. 

Paramedics tell you: “called for acute dyspnoea, I think it’s a COPD exacerbation, he is wheezing, I gave him bronchodilators and steroids, but he is worsening”.

He has a history of  COPD and hypertension. 

He presents sweaty, dyspneic, arterial pressure is high (220/110).

Physical examination is normal except for wheezing.

AP Chest X ray shows no signs of congestion.

Can you exclude an acute pulmonary oedema? 

Or something else than your stethoscope and x ray is needing? 

Conclusion 

Lung ultrasond has been shown to have greater diagnostic accuracy in differentiating the causes of acute dyspnoea in emergency settings compared with the traditional methods commonly employed in emergency departments (ED).

Its major advantages, particularly over radiographic tech- niques, are the absence of ionising radiation, speed and the fact that it is unaffected by the patient’s breath-hold limita- tions or agitation. 

The reliability of ULCs makes this method appealing for use in the emergency care setting. ULCs provide a direct, morphological, readily apparent imaging of abnormal increases in lung water. Recognition of diffuse interstitial involvement through B-line detection allows some pulmonary diseases to be rapidly ruled out, in particular, COPD exacerbation, which is one of the most common causes of acute dyspnoea. 

Bibliography 

Lichtenstein D, Mezière G (1998) 

A lung ultrasound sign allowing bedside distinction between pulmonary edema and COPD: the comet tail artifact. 

Intensive Care Med 24:1331–1334

L. Cardinale G. Volpicelli F. Binello G. Garofalo S.M. Priola A. Veltri C. Fava

Clinical application of lung ultrasound in patients with acute dyspnoea: differential diagnosis between cardiogenic and pulmonary causes

Radiol med (2009) 114:1053–1064

Lichtenstein DA (2007) 

Ultrasound in the management of thoracic disease. 

Crit Care Med 35:S250–S261

To be continued...

Ilenia Spallino

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Acute dyspnoea and X-Ray

It’s a dark night when a red code arrive at the ED by ambulance. 

Paramedics tell you: “called for acute dyspnoea, I think it’s a COPD exacerbation, he is wheezing, I gave him bronchodilators and steroids, but he is worsening”.

He has a history of  COPD and hypertension. 

He presents sweaty, dyspneic, arterial pressure is high (220/110).

Physical examination is normal except for wheezing.

AP Chest x ray shows no signs of congestion.

What about the LR of various chest x ray signs of congestion?

Conclusion 

Approximately 1 of every 5 patients with decompensated heart failure had no signs of congestion on ED chest radiography. Twenty percent of cardiomegaly observed on echocardiography is missed on chest radiography, and pulmonary congestion can be minimal or absent in patients with significantly elevated pulmonary artery wedge pressures. Although cephalization, interstitial edema, and alveolar edema were highly specific (96%, 98%, and 99%,respectively) for decompensated heart failure, their low sensitivity (41%, 27%, and 6%, respectively) makes them poor screening tools. The presence of congestion on chest radiography in ED patients with acute decompensated heart failure found a sensitivity of 81%. The presence of cardiomegaly has been shown to have moderate sensitivity (79%) and specificity (80%). Pleural effusion, when present, has been shown to be highly suggestive of acute decompensated heart failure in ED patients (sensitivity 25%; specificity 92%).

Clinicians should not rule out heart failure in patients with no radiographic signs of congestion

…and so what?

Bibliography 

Sean P. Collins, MD* Christopher J. Lindsell, PhD Alan B. Storrow, MD William T. Abraham, MD On behalf of the

Prevalence of Negative Chest Radiography Results in the Emergency Department Patient With Decompensated Heart Failure

ADHEREScientific Advisory Committee, Investigators and Study Group*

Annals of Emergency Medicine

Knudsen CW, Omland T, Clopton P, et al. 

Diagnostic value of B-type natriuretic peptide and chest radiographic findings in patients with acute dyspnea. 

Am J Med. 2004;116:363-368.

To be continued…

Ilenia Spallino

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Acute dyspnoea and clinical findings

It’s a dark night when a red code arrive at the ED by ambulance. Paramedics tell you: “called for acute dyspnoea, I think it’s a COPD exacerbation, he is wheezing, I gave him bronchodilators and steroids, but he is worsening”. He has a history of  COPD and hypertension. He presents sweaty, dyspneic, arterial pressure is high (220/110). Physical examination is normal except for wheezing.

What is the LR of clinical signs in the diagnosis of pulmonary oedema?

Conclusion 

The absence of pulmonary rales (sensitivity 0.60; specificity 0,78; LR + 2,73 LR – 0,51) and the presence of wheezing (sensitivity 0.22; specificity 0,58; LR+ 0,52 LR – 1,34) decreased the likelihood of heart failure insufficently to rule out a pulmonary oedema in a patient presenting with acute dyspnoea.

In acute setting you might  need something more than your stetoscope 

….but is it x ray?

Bibliography 

Does this dyspneic patient in the emergency department have congestive heart failure?

Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Department of Medicine, University of British Columbia, Canada.JAMA. 2005 Oct 19;294(15):1944-56.

To be continued…

Ilenia Spallino

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D-dimer and Aortic dissection

It’s 3.00 am when a 55 yo man is accompained to the ED by his wife because of sudden onset precordial pain, he has not clinical history, he does not smoke and he has an active life style, you find a normal blood pressure and clinical examination and a normal ECG, but the pain is severe and continuos. The patient start sweating, and you too. You give morfine and start thinking about….AORTA! you don’t find any pulse difference, but your feeling increases, how can you explain your feeling to the radiologist? 

Can something else help you to rule-out aortic dissection….

Conclusion The presence of pulse deficits or focal neurological deficits increases the likelihood of an acute thoracic aortic dissection in the appropriate clinical setting. Conversely, a completely normal chest radiograph result or the absence of pain of sudden onset lowers the likelihood. Overall, however, the clinical examination is insufficiently sensitive to rule out aortic dissection given the high morbidity of missed diagnosis. A negative D-dimer (<500) can rule-out an aortic dissection. Unfortunately a positive test does not give any additional chance to persuade radiologist… Bibliography Epidemiology of thoracic aortic dissection. LeMaire SA, Russell L. Nat Rev Cardiol. 2011 Feb;8(2):103-13. Epub 2010 Dec 21. Does this patient have an acute thoracic aortic dissection? Klompas M. JAMA. 2002 May 1;287(17):2262-72. Meta-analysis of usefulness of d-dimer to diagnose acute aortic dissection. Shimony A, Filion KB, Mottillo S, Dourian T, Eisenberg MJ. Am J Cardiol. 2011 Apr 15;107(8):1227-34. Epub 2011 Feb 4. D-dimer in ruling out acute aortic dissection: a systematic review and prospective cohort study. Eur Heart J. 2007 Dec;28(24):3067-75. Epub 2007 Nov 6. Sodeck G, Domanovits H, Schillinger M, Ehrlich MP, Endler G, Herkner H, Laggner A. D-dimer as the sole screening test for acute aortic dissection: a review of the literature. Sutherland A, Escano J, Coon TP. Ann Emerg Med. 2008 Oct;52(4):339-43. Diagnostic and prognostic value of circulating D-Dimers in patients with acute aortic dissection. Ohlmann P, Faure A, Morel O, Petit H, Kabbaj H, Meyer N, Cheneau E, Jesel L, Epailly E, Desprez D, Grunebaum L, Schneider F, Roul G, Mazzucotteli JP, Eisenmann B, Bareiss P. Crit Care Med. 2006 May;34(5):1358-64.  Ilenia Spallino

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